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Medical Officer Handbook for Neurosurgery

Department of Neurosurgery, Singapore General Hospital National Neuroscience Institute, Outram Campus Draft 2010

SY Lee S K Dinesh J Thomas June Goh


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TK Tan
Contents 1. Department Guidelines 1.1.1. Teaching programme 1.1.2. Weekly schedule 1. Neurophysiology 2. Neuroanatomy 2.1. Brain anatomy 2.2. Ventricular system
2.3.

Cerebral vasculature

3. Neuroradiology 3.1. CT, MRI , Angiography


3.2.

Neuroradiology scans

4. Neurological Examination 4.1. Mini Mental State examination 5. Relevant Neurology 5.1. Headache
5.2. 5.3. 5.4. 5.5. 5.6.

Hydrocepahalus Normal pressure hydrocephalus Status Epilepticus Herniations Brain death

6. Infections of the CNS 7. Spine


7.1. 7.2. 7.3. 7.4. 8.

Low back pain Treatment options Tethered cord syndrome Asia spinal association chart

Tumors

8.1. 8.2. 8.3. 9. 10.

Primary tumors Cerebral metastases Radiation therapy

Neurophthalamology Surgical procedures and Operations 10.1. Admission guidelines (Elective cases) 10.2. Craniotomy 10.3. Frameless Stereotactic surgery 10.4. External Ventricular Drain(EVD) 10.5. Ventriculo-peritoneal shunt(V-P shunt) 10.6. Omaya reservoir 10.7. Lumbar puncture 10.8. Lumbar drain 10.9. Transsphenoidal Pituitary Clinical Pathway 10.10. Stereotactic Radiosurgery Neurosurgical Trauma Management 11.1.1. Protocol for Management of Severe Head Injuries 11.1.2. Severe Head Injury protocol checklist 11.1.3. Barbiturate coma protocol 11.1.4. Commonly asked questions in head injury 11.1.5. Guidelines for the management of head injuries sustained after a fall by inpatients in SGH.

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12. SAH and aneurysms 12.1. Definition and grading of SAH 12.2. Management of Cerebral aneurysms 12.3. NICU SAH protocol 12.4. NICU SAH checklist
13.

Artriovenous malformations

14. Intracranial haemorrhage 15. Endocrinology


15.1.1. 15.1.2. 15.1.3. 15.2.

SIADH Cerebral salt wasting DI Fluids and Electrolytes

16. General ICU Care 16.1. Change of Tracheostomy 16.2. Central Line insertion 16.3. Inotropes
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16.4. 16.5. 16.6. 16.8. 16.9. 16.10.

Anaphylaxis Sedation Blood sugar control Oxygen therapy Eye Care Guidelines Deep Vein Thrombosis

16.7. Surgical Nutrition

16.11. Pulmonary Embolism 16.12. Advanced Monitoring 16.12.1. Cardio Q 16.12.2. Cerebral State Monitor 17. Neuropharmacology 17.1.1. Analgesia 17.1.2. Sedation 17.1.3. Antiepileptics 17.1.4. Antibiotics 17.1.5. Common Neurosurgery drugs 17.2. 17.3. Glossary Abbreviations

Department Guidelines Core curriculum for Medical Officers [Duration: 6 months] GENERAL OBJECTIVES: 1. To introduce the scope of neurosurgery to the medical officer by a combination of clinical exposure to neurologic disease, structured teaching, operating theatre experience, and academic/research projects. 2. To train the medical officer so that at the end of 6 months, he/she has achieved a certain level of competence and confidence in managing neurosurgical conditions. SPECIFIC OBJECTIVES: A. Clinical Skills 1. To be able to perform a competent neurological evaluation including pertinent details in history and neurological examination. 2. To understand and recognize the fundamentals of X-ray/CT/MRI/DSA imaging of the brain and spine, including normal appearances and common pathological lesions. B. Treatment / Management Abilities 1. Head trauma To diagnose and initiate management of the spectrum of mild, moderate and severe head injury. 2. Cerebrovascular disease To recognize and manage subarachnoid haemorrhage, intracerebral haematomas, and occlusive cerebrovascular disease, including investigations required, surgical decisions, treatment options and postoperative complications. 3. Neuro-oncology To understand the clinical features of primary and secondary CNS tumours, as well as treatment principles including types of investigations, indications for biopsy or resection, surgical techniques, and adjuvant therapy. 4. Spinal disease To evaluate, diagnose and manage acute spinal trauma, acute cord compression, degenerative spinal disease, neoplastic conditions of the spine and spinal dysraphism, including complications secondary to these conditions. 5. CNS infections To understand, recognize and manage brain abscesses, subdural empyema, shunt infections and wound infections. 6. Neuro-intensive care To manage a comatose neurosurgical patient in terms of ventilator support, ICP/CCP manipulation, fluid and caloric requirements, and infection control. C. Surgical Skills (to be taught and supervised) 1. Shunt tap / externalization For shunt infections or malfunction 2. Lumbar drain For CerebroSpinal Fluid (CSF) leak or control of ICP 3. Lumbar puncture 4. Central Venous Catheter insertion 5. Arterial line insertion

TEACHING PROGRAM Clinical / Surgical Experience Each medical officer will have exposure for 1 month in the following areas: 1. ICU 2. OT Structured Teaching 1. Weekly Journal Club presentations (Friday) Presentation of selected papers (classic and current).
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Weekly Morbidity & Mortality Round (Friday) Presentation and discussion on surgical morbidities and mortalities for audit, ensure good surgical practice, for learning and the prevention of mistakes from recurring. Weekly Rehab Rounds (Tuesday) Combined round with Neurosurgeon, physio/speech/occupational therapy, medical social worker, dietician and nurses, etc.

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4. Weekly NICU/Infectious Disease Rounds (Wednesday) Presentation and discussion with anesthetist and the ID physicians. 5. Weekly Neuro-Radiology Rounds (Friday) Combined conference with Neurologists and Radiologists on interesting clinical cases for management decisions.
6.

Weekly Grand Surgical Ward Rounds (Wednesday) Teaching rounds to review all in-house neurosurgical patients. Monthly Combined Neuro-Radiology / Neuro-Pathology Conference (Thursday) Combined conference with Neurologists, Radiologists and Pathologists on tumors, muscle and nerve biopsies.

7.

Academics / Research Projects Every medical officer will be encouraged to participate in a research project in one of the above 6 areas under the supervision of the various program directors. At the end of 6 months, the aim is for at least one of the following: Presentation of an abstract at a local / regional meeting Publication of a case report / study in a local / international journal

WEEKLY SCHEDULE Monday: Tuesday: Wednesday Morning (0800hrs-0900hrs): Weekly Rehab Rounds Morning (0800hrs-0930hrs): NICU surgical Grand Ward Round Afternoon (1300hrs-1400hrs):SICU/ NICU/Infectious Disease Round Thursday Afternoon(1700hrs-1800hrs):Neuro-Radiology/Neuropathology Rounds Morning(0900-1000hrs): Weekly Neuro-Radiology Rounds Afternoon(1400-1700hrs): Weekly Journal Club presentations Weekly Morbidity & Mortality Round

Friday:

Grand Ward Round: All neurosurgical patients are presented for review and discussion especially the cases in Neuro ICU (NICU) and Neuro ICA (NICA). It is an important learning opportunity for the junior staff. The GWR stamps should be stamped in the case notes and the decision made during GWR should be documented down inside the case notes. Mortality and Morbidity Round: The list for the mortality round is found in the Medical Officers (MOs) room. The purpose is to present and discuss surgical morbidities and mortalities for audit, ensure good surgical practice, for learning and the prevention of mistakes from recurring. It is an excellent learning opportunity for the junior staff. If in doubt of the management, please consult the neurosurgeon in charge of the case before the presentation. Present the relevant information. Tick the result of the discussion e.g. expected or unavoidable. Rectify any amendments in the template before submitting to the department secretary. Journal Clubs: The list of journals to be presented will be released the month before. If not, consult the consultant regarding the journals to be presented. MOs should start to prepare their presentation the week before their turn. Read up around the tropic itself to get a good grasp of the paper. Provide a summary of the paper including the relevant tables and charts. Do not present large amount of confusing data. Rehabilitation Round: Tuesday (0830hrs-0930hrs) This is a combined round with the neurosurgeon, physio/speech/occupational therapy, medical social worker, dietician and nurses etc. MOs will present a short history followed by discussion on the patients rehab issues, home plans, discharge plans etc. Neuro-radiology/Neuropathology Conference: Friday (0900hrs-1000hrs) Interesting cases are identified by the neurosurgeon during the course of the week for discussion during the X-ray conference. Cases to be identified and communicated to neuroradiologist by every Wednesday. Once a month, on the last Friday, there will be a
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combined neuroradiology/neuropathology round. Pathology cases to be identified and communicated to the pathologist one week prior to meeting. NICU/Infectious Disease Round: Wednesday (1300hrs-1400hrs) NICU cases will be presented for discussion with the anesthetist and the ID physicians. MOs can consult the ID physician individually if there are any issues in the ward after the round. Ward Coverage 1. 2. 3. 4. 5. A. B. NICU NICA Ward 52B Room 1, 2, 3, 4, 5 Over flow patients Operating Theatre Medical Officer (OT MO) (MO should have a roster among themselves to be inside OT) NICU will be covered by a different anesthetist on call in NICU every week. If in doubt always consult the NICU anesthetist on any procedures. NICU and NICA MOs cross cover each other for post call. NICU and NICA MOs should be aware and may need to manage the ICU and ICA beds requirement. There are 8 beds in the NICU (NES is sharing with Neuro Medicine). NICU MOs will need to notify Neuro Medical Registrar if NES needs to take over their beds. An afternoon round is usually done around 1600hrs in the NICU with the NICU MO, anesthetist and the on call MO to take over. C. Weekends, 3 MOs are requested to be present to do the rounds and to finish the changes before leaving. (Sat: at 1230hrs, Sun: after all changes are done).

D. One MO should be in the Ward at all times to cover the NICU patients. Procedures 1. All procedures (arterial line, lumbar puncture, central line, lumbar drain etc.) should be documented. Signed consent is required (except in cases of emergency when patient unconscious/ incompetent and no N.O.K. availabledocument your attempt to contact them). 2. CXR should be ordered after all ICU nasogastric tube insertions to document the tip is inside the gastric fundus. 3. If you have not performed a procedure before, please make sure you log 3 supervised procedures before getting clearance from the HOD to perform the procedures without supervision.

Neurophysiology Monro Kellie Model In a non-expansile, non-contractable (fixed), freely communicating space the pressure of the fluid contents is everywhere equal and directly proportional to the fluid volume. Intracranial pressure results from contributions from intracranial fluid compartments: 1. brain tissue (more than 80% fluid) 2. intra-arterial blood 3. cerebrospinal fluid (CSF). In the Monro-Kellie model total intracranial pressure is divided into a contribution from each of the 3 intracranial volumes: brain parenchyma, cerebrospinal fluid CSF, and cerebral arteries. The contribution of each compartment to the pressure is equal to the ratio of each compartment to the whole intracranial volume. As long as total intracranial volume stays the same the intracranial pressure remains the same. If the volume of one compartment increases or decreases the volume of one or both other compartment must decrease or increase in order for the total volume (and therefore, ICP) to remain the same. If the volume of any compartment is decreased while that of the other two volumes remains the same the total intracranial pressure must go down. The Monro Kellie model is the conceptual basis for current physical intracranial pressure management strategies and protocols. Cerebral perfusion pressure (CPP) The pressure the blood is under as it enters the cerebral arteries. This pressure is necessary to keep oxygenated blood from reaching the brain cells.
Cerebral perfusion pressure (CPP) = MAP [1/3(systolic pressure+2xdiastolic pressure)] ICP

Two major concepts underlie CPP/ICP resuscitation: the first is that elevated intracranial pressure decreases cerebral perfusion according to the equation CPP = MAP - ICP where "CPP" is "cerebral perfusion pressure", "MAP" = mean arterial pressure, ICP = intracranial pressure). Second, that there is a normal range for cerebral perfusion pressure and a threshold pressure at which cerebral perfusion is so low that cellular injury results. In management of increased intracranial pressure, an effort is made to maintain the ICP below 20 mmHg and the CPP above 60mmHg. Diuresis to decrease ICP should be avoided if there is any circulatory compromise either hypo or hyper-dynamic.

Intracranial Pressure The Monro Kellie hypothesis is the basis for reducing ICP by reducing the volume of: 1. brain and soft tissue, 2. intracranial circulating blood, 3. cerebrospinal fluid (CSF), or any combination of these. Soft tissue volume can be reduced by removal of tissue water with diuretics. Intravascular blood volume decreases when intracerebral blood vessels constrict in response to hyperventilation with alkalinization of the blood and CSF. The volume of the CSF compartment can be decreased directly by shunting and drainage. Monro Kellie Hypothesis (intracranial volume compartments)
Compartment Parenchyma Blood Cerebrospinal fluid % 70 5 25 Volume reduction technique Diuresis Hyperventilation Drainage

Management of Raised Intracranial Pressure 1. Head position around 30 degrees: Simple head elevation can promote venous return from the head and reduce ICP. It should be noted that head elevated does lower the mean arterial pressure supplying the brain, but the 30 degrees angulation has been shown to offer the best compromise. Hyperventilation: Though very effective in reducing ICP through its cerebral vasoconstrictive effect, hyperventilation causes reduced cerebral blood flow (CBF). Only mild to moderate degree of hyperventilation is recommended. (pCO2 > 30mmHg). Hyperosmolar agents: Mannitol can be used to draw water out of the brain tissue by osmotic forces. This reduces brain tissue volume and ICP. These agents should generally be "weaned off" to prevent rebound cerebral edema Sedation and pain relief. Agitation and muscle tremors/spasms can artificially elevate ICP. CSF drainage with an external ventricular drain can lower the ICP. Evacuate the causative intracranial mass lesion, including hematoma or neoplasm.

2.

3.

4.

5. 6.

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Ventricular System
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Circle of Willis (left) 1. Vertebral 2. Anterior Inferior Cerebellar 3. Basilar 4. Superior Cerebellar 5. Posterior Cerebral 6. Posterior Communicating 7. Middle Cerebral 8. Internal Carotid 9. Ophthalmic 10. Anterior Cerebral 11. Communicating 12. Hypothalamic 13. Anterior Choroidal

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Neuroradiology Computed Tomography(CT) CT scan looks at the intracranial tissues with a display greyscale (degrees of black and white) based on the density characteristics of the tissue volume.
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Plain x-rays and CT scans are images resulting from differential penetration of xrays through tissues of different densities. As on a plain x-ray, denser objects on CT are lighter, and less dense objects darker. On a cranial CT, bone is white, air is black, and brain tissue is intermediate shades of gray. The Hounsfield unit (named after one of the inventors of CT) quantifies the gradations from black to white on a density gray scale. Individual tissue types, such as gray matter, white matter, and fat, each have their characteristic Hounsfield value, which can be used to determine density (and, therefore, type) of tissue. Fat is very low density, even less than CSF: on CT it is closest in density of all tissues to air. Within the parenchyma, the darker areas are less dense, thus the gray matter of gross specimens appear lighter on CT than the corresponding gross white matter. We can use the Hounsfield unit measurement on our computer screen to determine the tissue types. CT is fast and cheap and good for bony definition but exposures pts to radiation and thus not suitable for pregnant women but is less sensitive for soft tissue differentiation.

Magnetic Resonance Imaging (MRI) MRI is more sensitive than CT for detection of lesions affecting the CNS, particularly those of the spinal cord, cranial nerves and posterior fossa structures Diffusion MR a sequence that detects reduction of microscopic motion of water, is the most sensitive technique for detecting acute ischemic stroke, useful in encephalitis, abscesses and prion diseases. Guidelines for neuroimaging Condition Haemorrhage Acute parenchymal Subacute/Chronic SAH Aneurysm Ischemic Infarction Haemorrhagic infarct Carotid/Vertebral Dissection Vertebral basilar insufficiency Carotid stenosis Suspected mass lesion e.g. tumors, abscess Vascular malformation White matter disorders, dementia Demyelinating disease Condition Cranial neuropathy, meningeal disease Infection, abscesses Immunosuppression with focal findings Seizures 1st time Partial complex/ refractory Trauma acute Shear injury/Chronic haemorrhage Spine stenosis
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Recommended technique CT>MRI MRI CT/CTA, LPAngio Angio>CTA,MRA CT MRI>CT MRI/MRA CTA, MRI/MRA CTA>Doppler U/S,MRA MRI + contrast MRI +/- Angiography MRI MRI +/- contrast Recommended technique MRI + contrast CT as screen MRI with coronal T2W imaging CT non-contrast MRI CT,MRI

Low Back pain without neurodeficits With deficits Cervical spondylosis Infection, myelopathy AVM

CT, MRI after 4 weeks of conservative Mx MRI>CT MRI or CT myelography MRI + contrast MRI, myelography, angiography

Conventional Angiography Invasive procedure, only reserved for pts in whom small vessel detail is essential for diagnosis and for whom interventional therapies are planned

Neuroradiology scans

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Extradural hematoma: lucid interval

Subdural hematoma: right hyperdense lesion, effacement of brain cortex (loss of gyri and sulci), left midline shift, compression of the ventricle

Acute hydrocephalus: CSF is produced continuously at a rate of approx 0.3ml/min, 20 ml/hr, 500 ml/day. Intraventricular volume CSF around 40ml. Total CSF volume at one time: 150 ml. Suddural Hygroma: preservation of the cerebral sulci and gyri. No need for treatment.

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Subarachnoid Hemorrhage (SAH): blood in the basal cisterna

Right chronic subdural Hematoma (SDH): right hyperdense acute on chronic SDH, with fluid level, midline shift towards the left, compression of the right lateral ventricle and effacement of sulci and gyri.

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Left Basal Ganglia Hematoma: mild midline shift to the right

Left thalamic bleed with intraventricular extension

Cerebellar hematoma

Angiogram: aneurysm in the left vertebral artery and spasm of basilar artery

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Towne Carotid 1. Internal Carotid 2. External Carotid 3. Anterior Cerebral 4. Middle Cerebral

Lateral Carotid 1. Internal Carotid 2. External Carotid 3. Anterior Choroidal 4. Anterior Cerebral

Towne Vertebral 1. Vertebral 2. Posterior Inferior Cerebellar 3. Anterior Inferior Cerebellar 4. Basilar 5. Posterior Cerebral

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Lateral Vertebral 1. Vertebral 2. Posterior Inferior Cerebellar 3. Basilar 4. Superior Cerebellar 5. Posterior Cerebral 6. Occipital 7. Posterior Temporal

Basic Neurological Examination Initial evaluation in the emergency setting. This is the basic information you will need before picking up the phone to consult the neurosurgical consultant. GCS initial, current (if different from initial). Time over which change occurred. Pupils symmetry/asymmetry, any change from initial findings. Limbs symmetry/asymmetry in GCS motor score, any change from initial findings. o If patient is obeying commands grade the power according to MRC grade BP, PR look for changes suggestive of a Cushings response (BP, HR). Complete Neurological Examination For all elective cases and as appropriate for urgent/ emergency admissions. The complete exam should be aimed for at least once, when the patient recovers sufficiently, during inpatient stay (if it was not done at admission). Cranial nerves I XII bilaterally 1. Olfactory occlude each nostril and ask the pt to gently sniff and correct identify a mild test stimulus. E.g. soap, toothpaste, coffee 2. Optic check visual acuity with or w/o correction with a Snellen chart. Map visual fields by confrontation in each quadrant in each eye, using a small white object moving form the peripheral towards the centre. Pts VF should be mapped against examiners. Formal perimetry and tangent screen exam may be necessary to document small defects. Refer Ophthalmologist if in doubt. Fundoscopy to view optic disc and note ratio. 3. 4, 6. Oculomotor, Abducens and - Direct and consensual papillary reaction to lightand convergence. Lid lag, droop, retraction. Range of movement of each eye. Left to right and then up and down. Document nystagmus if present. 5. Trigeminal Feel the masseter and temporalis when pt bites down and test jaw opening, protusion. Test sensation over entire face and document which division(Ophthalmic,VI- forehead; Maxillary,V2- cheek; Mandibular,V3-lower lip). Test Cornea(V1) with a small wisp of cotton for sensation. Test jaw jerk. 7. Facial Asymmetry of face at rest. Test eyebrow elevation, forehead wrinkling, eye closure, smiling, frowning, puffing of cheeks, whistle. Check if forehead is spared (in UMN lesions). Test for taste in anterior 2/3 of tongue( cotton bud soaked in 50% glucose). Test tear production from lacrimal glands (Schirmer test) . 8. Vestibulocochlear- Ability to hear tuning fork, finger rub, watch tick. Rinnes test(516Hz tuning fork on mastoid process{BC} then in front of ear{AC}, ask which is louder) and Webers test(516Hz tuning fork on vertex of head, ask which ear is louder). Otoscopy to examine tympanic membrane. Rinne test in deaf ear Webers test Conductive dearness Bone Conduction,BC>AC Deaf ear louder Sensorineural deafness Air Conduction,AC>BC Good ear- louder

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9. 10. Glossopharyngeal and Vagus -Palate-uvula elevation with ahhh sensation in posterior pharynx, tonsils and posterior 1/3 taste sensation in tongue. Gag reflex on each side. Direct examination of vocal cords by laryngoscopy by ENT if necessary 11. Accessory check shoulder shrug(trapezius) and head rotation(SCM) to each side 12. Hypoglossal check bulk and power of tingue. Look for deviation form midline on protusion, fasciculations and atrophy. Tone, power, reflexes (deep tendon + plantar), sensation in all limbs Medical research council(MRC) scale 5 normal,4-submaximal power against resistance, 3 antigravity movement, 2- movement with gravity eliminated, 1- flicker of movement, 0- none Tone normal, decreased, increased spastic, lead pipe, cogwheel Reflexes C5-Biceps; C6-Supinator; C7-triceps,C8-finger;L3/4-knee;S1-ankle Sensation- light touch, pain, and temperature should be tested separately. Refer to Asia spine association chart and anatomy diagram for dermatomes (page) Cerebellar function assessment Rapid alternating movements (Dysdiadochokinesia) tapping one hand on the back of the other quickly; demonstrate to pt 1st. Finger nose test- look for past pointing (dysmetria), intention tremor Heel-shin test joint position sense, movements are worse when repeated with eyes closed Gait Rombergs, veering to side of lesion(cerebellar ataxia) Speech- slurring, disjointed rhythm with scanning speech Nystagmus multidirectional gaze-evoked in cerebellar lesions- nystagmus in the direction of gaze, occurring in more than one direction In patients with skull base fracture: assess for CSF leak (if not initially obvious, reassess when patient is able to sit up in temporal bone fracture assess hearing + facial nerve function. In trauma cases assess cervical spine clinically + radiologically. CT/MRI C-spine if necessary.

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Mini mental examination Mental status exam is an important diagnostic tool used to evaluate a patient's orientation, concentration and memory (i.e. cognition). Although it is not imperative to perform a mini mental exam each time you evaluate a patient neurologically, a baseline score should be established when a patient is first examined. Serial exams may be performed if deficits in cognition are noted at a later date or discovered upon the initial examination. More in-depth neurocognitive tests may be necessary if deficits are discovered. The mini mental exam is scored out of a total of 30 points. A score of 24 or higher is considered within normal range, although specific deficits may be noted and investigated further. A score of below 24 is indicative of dementia. Performance of the mini mental examination.

Orientation. Date: Ask the patient to state the date. The patient achieves one point for each correct answer of the following: year, month, day, season and numerical date (a total of five points). Location: Ask the patient to state where they are. The patient achieves one point for address, town, country, hospital and ward (a total of five points) Registration. Ask the patient if you can test their memory. State the name of three unrelated items (dog, pencil, ball) and then ask the patient to repeat the three items. The patient gets one point for each item repeated, i.e. registered (a total of three points). Ask the patient to remember these items, because you will ask for the patient to repeat them again later in the examination. Attention and Calculation. Ask the patient to begin with 100 and count backwards by subtracting 7's. The patient receives 1 point for each correct answer with a maximum of five points. If the patient is unable to subtract, have them spell the word WORLD in reverse, getting 1 point for each correct letter. Recall. Ask the patient to repeat the three words that they were asked to remember.Score 0-3. Language. Naming: Show the patient a watch and then ask them to name the object shown to them. Repeat this question showing the patient a pen. Score 0-2. Repetition: Ask the patient to repeat the following sentence: "No ifs, ands, or buts." Score 0-1.

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Three step command: Hand the patient a piece of paper and state the following command: "hold this piece of paper, fold the paper in half, place the paper on the table". One point for each correct movement, maximum of 3. Reading: On a blank sheet of paper write clearly the following: CLOSE YOUR EYES. Show this paper to the patient and ask them to read it to themselves and do what it says. Score 0-1. Writing: Give the patient a piece of paper and pen and ask the patient to write any sentence they would like. The sentence must contain a noun and a verb, yet correct punctuation is not required. Score 0-1. Copying: On a sheet of paper draw two intersecting pentagons and then ask the patient to copy these objects. Score 0-1. All ten angles must be present with appropriate intersection points. Ignore tremor. Consciousness. Estimate the patient's level of consciousness: alert, lethargic, obtunded, stuporous, or comatose. An alert patient is vigilantly attentive and keen. A lethargic patient is dull, sluggish and appears half asleep. An obtunded patient opens their eyes, responds slowly to questions, is somewhat confused, and has a decreased interest in their environment. A stuporous patient is near unconscious with apparent mental inactivity and reduced ability to respond to stimulation. Comatose patients are unconscious and unresponsive.

Add the up the total score and note the level of consciousness.

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Relevant Neurology Headache Chronic recurring headache Vascular type : migraine Muscular : tension headache Headache due to pathology Intracranial pathology: Subarachnoid haemorrhage sudden onset severe headache, worst head of my life with vomiting and focal neurological deficits Increased ICP from any cause Tumor causing mass effect or hydrocephalus Irritation or Inflammation of the meninges : meningitis Local pathology Eye pain , frontal sinusitis, giant cell arteritis Head trauma post concussive syndrome Following craniotomy Any new severe headaches or a change in pattern of a long-standing, recurrent headache warrants a CT or MRI brain especially when accompanied with symptoms of nausea and vomiting and or a abnormal neurological exam. Post LP headache A.k.a spinal headache. Follows procedures like lumbar puncture/drain or dural opening. Occurs when patient is erect and relieved when recumbent. May be associated with nausea, vomiting, visual disturbances and dizziness Pathophysiology It is thought to be due to CSF leakage due to dura puncture which reduces the CSP cushioning effect on the brain, accompanied with gravity pull on the brain when erect, tension and traction on the dura blood vessels and tethering of the brain to the pain sensitive dura. Occurs in about 20% after LP. Treatment Lie flat in bed for at least 6 hrs Maintain good hydration, PO or IV Analgesia e.g. paracetamol 1g QDS/PRN Abdominal binder High dose sterioids : PO dexamethasone 20mg/day and tail down the dose gradually Epidural blood patch : Access the epidural space, separate sterile venepuncture site to withdraw 10mls of patients own blood and inject it into the epidural space. Ensure that one is in the epidural space and ensure that CSF cannot be aspirated prior injection. Lie for 30mins supine. Effective in one application in 90%, may be repeated if ineffective. Risks : infection, cauda equine compression.

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Hydrocephalus Hydrocephalus is a condition in which excess CSF builds up within the ventricles of the brain and may increase pressure within the head. CSF has three crucial functions: 1) it acts as a "shock absorber" for the brain and spinal cord; 2) it acts as a vehicle for delivering nutrients to the brain and removing waste; and 3) it flows between the cranium and spine to regulate changes in pressure within the brain. The average adult produces about 300mls of CSF daily. When an injury or illness alters the circulation of CSF, one or more of the ventricles becomes enlarged as CSF accumulates. In an adult, the skull is rigid and cannot expand, so the pressure in the brain may increase profoundly. Hydrocephalus is a chronic condition. It can be controlled, but usually not cured. With appropriate early treatment, however, many people with hydrocephalus lead normal lives with few limitations. Hydrocephalus can occur at any age, but is most common in infants and adults age 60 and older. It affects adult males and females, as well as people of different races about equally. Experts believe that normal pressure hydrocephalus accounts for 5 to 6 percent of all cases of dementia. Hydrocephalus Ex-Vacuo Hydrocephalus ex-vacuo occurs when a stroke or injury damages the brain and brain matter actually shrinks. The brain may shrink in older patients or those with Alzheimer's disease, and CSF volume increases to fill the extra space. In these instances, the ventricles are enlarged, but the pressure is usually normal. Symptoms of Adult-Onset Hydrocephalus Headaches Nausea Difficulty focusing the eyes Unsteady walk or gait Leg weakness Sudden falls Irritability Drowsiness Personality changes Seizures

Diagnosing Hydrocephalus Review pts medical history, and perform a complete neurological examination including diagnostic testing if needed Ask specific questions to determine if symptoms are caused by hydrocephalus

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The neurological examination will also help to determine the severity of your condition. There are a wide variety of diagnostic tests that can help pinpoint the cause and severity of hydrocephalus. These include Computed tomography scan (CT scan),Magnetic resonance imaging (MRI), Isotopic cisternography, Lumbar puncture , Intracranial pressure monitoring

Surgery Hydrocephalus can be treated in a variety of ways. The problem area may be treated directly (by removing the cause of CSF obstruction), or indirectly (by diverting the fluid to somewhere else e.g. V-P,V-A shunt). Indirect treatment is performed by implanting a shunt to divert the excess CSF away from the brain. The body cavity in which the CSF is diverted is usually the peritoneal cavity In some cases, two procedures are performed, one to divert the CSF, and another at a later stage to remove the cause of obstruction (e.g., a brain tumor). Once inserted, the shunt system usually remains in place for the duration of a patient's life (although additional operations to revise the shunt system are sometimes needed). The shunt system continuously performs its function of diverting the CSF away from the brain, thereby keeping the intracranial pressure within normal limits. An alternative operation called endoscopic third ventriculostomy may be recommended. In this operation, a tiny burr hole is made in the skull and a neuroendoscope is utilized to enter the brain. The neurosurgeon will then make a small hole in the floor of the third ventricle, creating a new pathway through which CSF can flow. Prognosis The prognosis for hydrocephalus depends on the cause, the extent of symptoms, and the timeliness of diagnosis and treatment. Some patients show a dramatic improvement with treatment while others do not. In some instances of NPH, dementia can be reversed by shunt placement. Other symptoms such as headaches may disappear almost immediately if the symptoms are related to elevated pressure. If the cause of NPH is known, the rate of shunting success can be as high as 80 %. In cases in which the cause is unknown, the success rate varies from 25-74%. In general, the earlier hydrocephalus is diagnosed, the better the chance for successful treatment. The longer the symptoms have been present, the less likely it is that treatment will be successful. There is no way to accurately predict how successful surgery will be for each individual. Some patients will improve dramatically while others will reach a plateau or decline after a few months. Shunt malfunction or failure may occur. The valve can become clogged or the pressure in the shunt may not match the needs of the patient, requiring additional surgery. In the event of an infection, antibiotic therapy may be needed. A shunt malfunction may be indicated by headaches, vision problems, irritability, fatigue, personality change, loss of coordination, difficulty in waking up or staying awake, a return of walking difficulties, mild dementia or incontinence.

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Normal Pressure Hydrocephalus (NPH) First described in 1965, A.k.a Hakim-Adams syndrome. Occurs in > 60 years old, more in males. Key features 1. Classic triad of Dementia, Gait disturbances and urinary incontinence 2. Communicating hydrocephalus on imaging, CT/MRI 3. Normal pressure on LP 4. Symptoms relieved after CSF shunting Etiology 1. Post SAH/ Post-trauma 2. Post-meningitis 3. After posterior fossa surgery 4. Tumors 5. Associated with Alzheimers disease (15%) 6. Deficiency of arachnoid granulations 7. Overlooked aqueductal stenosis 8. Idiopathic Diagnosis 1. LP pressure < 18cm H20; Response to a single/serial LP may be predictive 2. Trial of Lumbar drain (5 days, Mean improvement time 3 days) 3. Communication hydrocephalus on imaging 4. Others : EEG, CBF measurements( not specific), radionuclide cisternography Management 1. Dementia work-up should be completed 2. VP shunt is the treatment of choice( See page ..) 3. Medium pressure(65-90mmHg) valves should be used to prevent risk of SDH 4. Post-op, gradually sit the patient up slowly over a period of days. 5. If no improvement, assess for shunt malfunction. 6. Follow-up clinically and with CT/MRI 6-12 monthly Complications 1. SDH, hygroma, higher risk with low-pressure valves 2. Shunt infection 3. Shunt malfunction/migration 4. Intraparenchymal haemorrhage 5. Seizures Outcome 1. Urinary incontinence is the most likely to response to shunt, followed by gait disturbance and lastly dementia

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2. 3.

Prognosis is better when symptoms are present for a short period Some do not improve and continue to deteriorate, it is important to exclude shuntrelated problems before attributing it to the natural course of disease.

Status Epilepticus Definition Defined as continuous seizure activity of more than 30 mins or 2 or more seizures without restoration of conciousness in between. If the seizure duration has exceeded 4 mins, then steps must be taken to abort the seizure. Aetiology CNS infection, trauma, tumour, CVA, anoxia etc Investigations 1. CT scan or MRI head in patients with new onset status and those with focal seizures 2. Lumbar puncture when an infectious etiology or SAH not seen on CT scan is being suspected 3. EEG: useful in determining whether the patient has a generalized or focal epileptiform abnormality and in helping to diagnose a non-convulsive status 4. Metabolic and toxicology screen and anticonvulsant levels Immediate management ABCs: Protect airway (roll patient on side, insert oral/nasal airway if possible, with supplemental O2; breathing and circulation) 2) Cardiac monitoring, SpO2 monitoring, ECG 3) IV access and sent bloods for FBC, U/E/Cr, Ca2+, Mg+, PO4-, Hypocount stat 4) Toxicology, ABG and therapeutic drug levels if indicated 5) Protocol to abort fit a) Give I/V diazepam 10mg bolus, max 20mg. PR Diazepam 10 mg if no IV access i) Give 5mg at a time, If there is any evidence of respiratory depression, stop infusion and transfer patient to ICU. b) DO NOT GIVE IF THE SEIZURE HAS ALREADY STOPPED. c) Diazepam should usually be followed by phenytoin loading. d) If not previously on phenytoin. Load with IV phenytoin 15mg/kg up to 1000mg in N/S not dextrose solution (to prevent precipitation) infuse at max rate of 50mg/min (1gm over 20 mins) with ECG monitoring. Stop/slow the infusion rate if there is any arrthymias i.e. QRS widening or hypotension. If the patient is on phenytoin and the level is not known, give IV phenytoin 500mg at 50mg/min. If patient is allergic to phenytoin use valproate. e) If seizures were to continue, transfer patient to ICA/ICU. f) Give additional dose of phenytoin at 5mg/hr up to 30mg/kg g) If seizure still persistent, inform the intensivist. h) Start phenobarbitone 10mg/kg at < 100mg/min up to 20mg/kg. Reduce the infusion rate if the BP falls.
1)

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i) If the seizures are still persistent, the patient may need a general anesthetic and/or barbiturate coma. This rare situation is to be co-managed with the intensivist and the neurologist. Note: In alcoholics and patients in whom hypoglycemia is identified as a cause, IV thiamine 50-100mg should precede the glucose bolus. 6) Treat the precipitating cause Anticonvulsants in prophylaxis and treatment of Seizures Phenytoin Loading dose: oral: 300 mg tds for 1 day. IV : 1g (up to 15 mg/kg) neat solution diluted to 20ml in N/S given over 20 minutes (i.e. rate not exceeding 50mg per minute) at the bedside by the M.O. with concurrent ECG monitoring. Maintenance doses of about 100mg should be given thereafter at intervals of every 68 hours, monitored by measurement of plasma concentrations; rate and dose reduced according to weight Watch for hypotension or arrythmias. Stop/slow down infusion rate if this is observed. To avoid local venous irritation each injection or infusion should be preceded and followed by an injection of sterile physiological saline through the same needle or catheter by intravenous injection via caval catheter, 3.55 mg/kg at a rate not exceeding 50 mg/minute, with blood pressure and ECG monitoring; repeat once if necessary By intramuscular injection, not recommended Sodium valproate Contraindications liver dysfunction, pancreatitis, porphyria, blood disorders. Dilute in Normal saline 0.9% Loading dose: i.v. 400-800mg slow I.V. (up to 10 mg/kg) Infuse over 3-5 minutes. Followed by iv infusion @ 1-2mg/kg/hr up to 2.5g/day Monitor liver function before and after initiation of therapy. For both drugs moderate dosage in patients who are hypoalbuminemic (common after severe illness). Consult the pharmacist about this.

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Herniations Brain herniation represents mechanical displacement of normal brain relative to another anatomic region secondary to mass effect from traumatic, neoplastic, ischemic, or infectious etiologies. Herniations of the brain are divided in 5 major categories: (1) transtentorial, (2) subfalcine/cingulate, (3) foramen magnum/tonsillar, (4) sphenoid/alar, and (5) extracranial. Each category of herniation is associated with a specific neurologic syndrome. Transtentorial herniation Transtentorial herniation is a downward or an upward displacement of the brain through the tentorium at the level of the incisura. A descending transtentorial herniation occurs when the supratentorial brain herniates downward through the incisura. An ascending transtentorial herniation occurs when the infratentorial brain herniates upward through the incisura. Descending transtentorial herniation occurs more often than ascending herniations and includes the subcategory of uncal herniation. Ascending transtentorial herniation usually results from a posterior fossa tumor with mass effect. This results in the distortion of the midbrain, flattening of the posterior quadrigeminal plate and narrowing of the bilateral ambient cisterns. Extra-axial or intra-axial hematomas of the posterior fossa is a less common cause. Descending transtentorial herniation can cause various symptoms. Compression of the ipsilateral cranial nerve III may lead to ipsilateral dilatation of the pupil and abnormal extraocular movements. Compression of the ipsilateral corticospinal tracts in the brainstem may cause contralateral hemiparesis because these tracts decussate at the level of the medulla. Ipsilateral hemiparesis can also occur if there is sufficient mass effect causes the contralateral cerebral peduncle (Kernohan notch) to be compressed against the adjacent incisura. Other complications include unilateral or bilateral occipital lobe infarction from compression of the posterior cerebral artery. Brainstem hemorrhages are other complications caused by compression or kinking of pontine perforating vessels. Compression on the midbrain may cause hydrocephalus. Ascending transtentorial herniation causing brainstem compression can cause nausea and vomiting, which may progress rapidly to coma if rapid changes occur in the intracranial anatomy. A slow-growing mass in the posterior fossa results in slow changes in the intracranial anatomy; these do not often present as an acute emergency. Subfalcine/cingulate herniation

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Subfalcine herniation occurs when the supratentorial brain is displaced underneath the falx secondary to mass effect. Subfalcine herniation does not necessarily indicate severe clinical symptoms. This type of herniation may lead to the clinical findings of headache, and symptoms may progress to contralateral leg weakness or ipsilateral frontal lobe infarction secondary to compression of the anterior cerebral artery. Foramen magnum/tonsillar herniation Foramen magnum herniation occurs when the infratentorial brain is displaced through the foramen magnum secondary to mass effect. Acute compression of the brainstem may result in obtundation and death. However, patients with Chiari I malformation may present with a paucity of symptoms, or they may present with dysesthesia in the extremities with cervical flexion. This is referred to as Lhermitte phenomenon Sphenoid/alar herniation Sphenoid/alar herniation results from the supratentorial brain sliding either anteriorly or posteriorly over the wing of the sphenoid bone. An anterior herniation occurs when the temporal lobe herniates anteriorly and superiorly over the sphenoid bone. Conversely, a posterior herniation occurs when the frontal lobe herniates posteriorly and inferiorly over the sphenoid bone. Associated clinical symptoms are usually minimal, though sphenoid herniations are often associated with other types of herniations. Extracranial herniation Extracranial herniation occurs with displacement of brain through a cranial defect. This finding usually results from a traumatic or surgical cause. The herniated region of the brain may become ischemic, leading to infarction. Invesitgations: For transtentorial herniation, CT or MRI is useful for evaluation. MRI can provide axial as well as sagittal and coronal views. Intervention Medical Treatment to decrease intracranial pressure. E.g. mannitol, hyperventilation, steroids etc. Surgical intervention in the treatment for increased intracranial pressure is dependent on cause. Neoplasms causing brain herniation may be resected if possible, to reduce mass effect. Patients with a large parenchymal and extra-axial hemorrhage may benefit from a standard craniotomy or craniectomy with duraplasty followed by clot evacuation. In cases of descending transtentorial herniation of the brain caused by a large subdural hematoma, emergency surgical decompression is required to prevent irreversible injury to the brainstem, as well as other areas of the brain.

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Brain Death Brain death refers to the total and irreversible cessation of all functions of the brain. A person who is brain dead has no spontaneous respiration and will need to be supported on a ventilator. Brain death is accepted as a legal definition of death in Singapore and in other advanced countries. It is determined based on a well-defined standard set of clinical criteria. The seven clinical criteria for determining irreversible cessation of all functions of the brain are as follows:
1. 2. 3. 4. 5. 6. 7. the pupils are fixed and non-reactive to strong light there is no corneal reflex; there is no spontaneous motor response to painful stimulus, excluding spinal reflexes, there is no oculeocephalic reflex; there is no gag reflex or reflex response to tracheobronchial stimulation; there is no vestibule-ocular response on instillation of 50 cubic centimetres of ice-cold water into each ear; and there is no spontaneous respiration even with carbon dioxide tension at 50 millimetres or more or mercury.

These tests are to assess whether there is any response to various physical stimuli such as light, touch and pain. Brain death can only be certified if all seven clinical criteria are met. The clinical criteria for brain death as specified in the Interpretation Act must be observed to be present in the patient separately by two doctors before brain death can be certified. Both doctors must be experienced with specialist qualifications. Should the two doctors have differing opinions, brain death would not be certified. The two doctors who examine the patient must:

not have been involved in the care or treatment of the patient being certified not belong to the team of medical practitioners who will remove the organ from the body not have been involved in the selection of the proposed recipient of the organ not be involved in the care or treatment of the proposed recipient of the organ during his hospitalisation for the transplant

The following supplementary tests are allowed to be used for brain death certification. 1. Cerebal angiography to confirm that there is no intracranial blood flow. 2. Radionuclide scan to confirm that there is no intracranial profusion. The supplementary tests are to complement the clinical tests. They are not a substitute for the clinical criteria. If six of the seven clinical tests can be performed, the criteria for these six tests must be fully met, that is 6 upon 6, before the doctor proceeds to carry out an ancillary test.

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Infections of the CNS

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Acute infections include bacterial meningitis, viral meningitis, encephalitis, focal infections e.g. abscess, subdural empyema. Medical emergency, treatment should commence once suspected. Key goals 1. Identify and distinguish between the different conditions 2. Identify the pathogen 3. Initiate appropriate antimicrobial therapy and institute surgical treatment if necessary Clinical Presentation 1. Acute Rapid onset(<24-48hrs) of headache, fever and/or meningismus(nuchal rigidity), impairment of higher functions e.g. lethargy to coma. Commonly from pyogenic meningitis ( Strept. Pneumoniae, Nesseria meningitides, Haemophillus influenzae) 2. Subacute - >48 hr onset with gradual worsening symptoms, with no or gradual impairment of higher functions. Commonly viral or granulomatous in origin. History 1. Risk factors prior infection e.g. otitis, sinusitis, pneumomia, endocarditis, asplenia, sickle cell, multiple myeloma, alcoholism, cirrhosis, head trauma with CSF leak, immunocompromised state e.g. AIDS, transplant pts, chronic steroid therapy 2. Listeria monocytogenes is a important consideration in pregnant women 3. Previous invasive neurosurgical procedure, think of S. aures, coagulase-negactive staphylococcus. 4. Rash of meningococcemia begins as a maculpaplular rash developing into a petechial rash on trunk, lower extremities, mucous membranes, palms, soles Principles of Management 1. Initiate empirical therapy once bacterial meningitis is suspected. Antibiotics should be started w/i 30mins. IV Ceftriaxone 2g stat, continue with 2g bd x 7-10 days. Consider adding amikacin if there is risk of CSF leak. Chloramphenicol if allergy to penicillin. Consult ID if in doubt. 2. Perform septic work-up including LP. If focal neurology or papilledema or signs of raised ICP, obtain CT head first. CSF for FEME, C/S, AFB smear and gram stain, viral serology/PCR if suspected .Bloods for FBC, U/E/Cr, PT/PTT, GXM , ESR, CRP. CXR, Urine C/S and UFEME. 3. If suspect viral encephalitis, give IV acyclovir(10mg/kg 8hrly for 14 days) for presumptive herpes simplex.( Obtain MRI +/- EEG). HSV affects temporal lobes mainly. 4. CLC, Hrly parameters, admit to ICU/ICA, Intubate if GCS < 8. obtain ID consult early. 5. Treat seizures with Phenytoin . 6. Treat TB Meningitis with isoniazid(15mg/kg/day), rifampicin(15mg/kg/day), and pyrazinamide(1.5-2g/day) CSF findings in Meningitis Cause/CSF Appearance WBC/mm3 Type of wbc Protein Glucose

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Normal Viral Bacterial TB

Clear Clear Cloudy Clear

<3 <200 >1000 <200

Lymphocytes >60% Polymorphs Lymphocytes

g/L 0.2-0.4 <0.1 >0.1 >0.1

mmol/L > 2.2 >2.2 <2.2 <2.2

Viral Meningitis/ Encephalitis Presents less acutely compared to bacterial cause. CSF lymphocytic pleocytosis. Malaise, myaglia, nausea, vomiting and a mild degree of lethargy, drowsiness may occur. Encephalitis has more impairment of higher function e.g. altered consciousness, aphasia, hemiparesis, cranial nerve defects to coma. Enteroviruses account for 75-90% of aseptic meningitis. These include Coxsackie, echoviruses, polio and human enteroviruses. Herpes simplex virus(HSV) type 2, arboviruses and HIV are also common. Diagnosis is via CSF examination and PCR, viral C/S Supportive treatment with IV acyclovir for HSV, EBV, VZV if indicated. Brain abscess Focal, suppurative infection w/i the brain parenchyma, typically surrounded by a vascularised capsule. Risks factors are immunocompromised hosts, prior infections, invasive neurosurgical procedures, head trauma. In immunocompromised host, most are caused by fungi and parasites, less of bacteria e.g. Toxoplasma gondii, Aspergillus, Norcardia, Mycobacteria, Cryptococcus neoformans. MRI is better than CT. Appears on CT as a focal mass with ring enhancement. DWI sequencing can help in differentiating focal lesions e.g. tumors vs abscess. Abscess typically show increase signal and low apparent diffusion coefficient. Microbiological diagnosis is best achieved by C/S, gram stain of stereotactic biopsy of abscess material. Blood C/S positive in 10%. CSF is not helpful

Low Back Pain

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An estimated 75 to 85 percent will experience some form of back pain during their lifetime. In about 90 percent of all cases, pain improves without surgery. However, 50 percent of all patients who suffer from an episode of low back pain will have a recurrent episode within one year.

Common Causes of Low Back Pain

Herniated Disc (slipped disc) A herniated disc is a fragment of the disc nucleus pulposus that is pushed out of the annulus into the spinal canal through a tear or rupture. Activity, aging or a mechanical problem in the spine can cause one of the discs to bulge. Irritation or pressure may cause back pain that radiates down the back of one or both of the legs (sciatica).There may be numbness or weakness of the affected nerve roots. The key to initial treatment is to relieve the nerve root pressure or irritation.

Disc degeneration (osteoarthritis of the spine) One of the most common disorders of the lower spine is disc degeneration, or osteoarthritis of the spine. As the body ages, the discs in the spine dehydrate. The bones and ligaments also undergo degeneration. Degeneration in the discs is not uncommon.. Pain occurs when the discs become compressed and exert pressure on the nearby nerve roots or spinal cord. Treatment options for patients with degenerative disc disease in the spine range from simple analgesia, to physiotherapy to epidural steriod injections to surgery.

Lumbar spinal stenosis Lumbar spinal stenosis (LSS) is a narrowing of the spinal canal which compresses the nerves exiting through the foramina. The discs may become less spongy as you age, resulting in reduced disc height and bulging of the hardened disc into the spinal canal. Patients who suffer from LSS often experience pain and weakness in the legs and a dull pain in the lower back. Sometimes, relief is obtained by sitting or by bending over while standing. Pain, numbness and weakness typically get worse when patients are standing erect or walking. Many patients respond well to conservative treatment for several years. Surgical treatment focuses on opening up the spinal canal and relieving pressure on any nerve roots that are being irritated.

Spondylolisthesis

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Degenerative spondylolisthesis is caused by osteoarthritis of the facet joints. Most commonly, this involves the L4 slipping over the L5 vertebra. It is usually treated with the same conservative and surgical methods as lumbar spinal stenosis.

Diagnosis History, physical examination, Investigations e.g. X-rays, CT scan MRI, Myleogram, Discography, Electromyogram and Nerve Conduction Studies (EMG/NCS)

Conservative Treatment Options Treatment options include physical therapy, back exercises, weight reduction, steroid injections (epidural steroids), nonsteroidal anti-inflammatory medications, rehabilitation and limited activity. At least four to six weeks of conservative therapy should be tried before considering surgery.

Indications for Surgery When conservative treatment for low back pain does not provide relief, surgery may be considered. These are several considerations e.g. Back and leg pain limits normal activity or impairs quality of life, progressive neurological deficits, bowel and bladder dysfunction If surgery is recommended, a variety of options are available to help relieve pressure on the nerve roots.

Surgical Procedures

Anterior Lumbar Interbody Fusion (ALIF): Removal of the degenerative disc by going through the lower abdomen. Bone graft material or a metal device filled with bone is then placed into the disc space. Foraminotomy: Surgical opening or enlargement of the bony opening traversed by a nerve root as it leaves the spinal canal, to help increase space over a nerve canal. This surgery can be done alone or together with a laminotomy. Laminotomy: An opening made in a lamina, to relieve pressure on the nerve roots. Laparascopic Spinal Fusion: A minimally invasive procedure involving small incisions in the abdomen, through which a graft is placed into the disc space. Medial Facetectomy: Surgical procedure to remove part of the facet (a bony structure in the spinal canal), to increase the space. Posterior Lumbar Interbody Fusion (PLIF): Removal of the posterior bone of the spinal canal, retraction of the nerves, and removal of the disc material from within the disc space, followed by insertion of bone graft and sometimes hardware

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in order to fuse the bones. This procedure is called an "interbody fusion" because it is performed between the "bodies" of the vertebral bones and across the diseased disc space. This procedure is typically performed on both sides of the spine. Posterolateral fusion: Placing bone on the back and side of the spine to achieve a fusion. Transforaminal Lumbar Interbody Fusion (TLIF): Removal of the posterior bone of the spinal canal, retraction of the nerves, and removal of the disc material from within the disc space, followed by insertion of bone graft and sometimes hardware in order to fuse the bones. Similar to a PLIF, but frequently performed from only one side.

The benefits of surgery should always be weighed carefully against its risks.

Tethered Spinal Cord Syndrome Myelomeningocele/Lipomyelomeningocele Tethered spinal cord syndrome is a neurological disorder caused by tissue attachments that limit the movement of the spinal cord within the spinal column. These attachments cause an abnormal stretching of the spinal cord. Closely associated with spina bifida. Estimated that 20-50% of children with spina bifida defects repaired shortly after birth will require surgery at some point to untether the spinal cord. In people with spina bifida (myelomeningocele), the spinal cord fails to separate from the skin of the back during development, preventing it from ascending normally, so the spinal cord is low-lying or tethered. In patients with a lipomyelomeningocele, the spinal cord will have fat at the tip and this may connect to the fat which overlies the thecal sac As the child continues to grow, the spinal cord can become stretched, causing damage and interfering with the blood supply to the spinal cord. Primary Causes In addition to myelomeningocele and lipomyelomeningocele the other causes are: Dermal sinus tract Thickened/tight filum terminale Diastematomyelia history of spine trauma Lipoma history of spine surgery Tumor Symptoms Skin discoloration on the lower back Hairy patch on the lower back Back pain, worsened by activity and relieved with rest Leg pain, Lower limb neurological deficits e.g. numbness, weakness

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Deterioration in gait Progressive or repeated muscle contractions Leg deformities Spine tenderness Scoliosis Bowel and dysfunction

Diagnosis History, Physical examination. Imaging.If a tethered cord is suspected, one or more tests may be necessary to confirm the diagnosis e.g. MRI, Myleogram, CT scan, Ultrasound. Surgery Untethering is generally performed only if there are clinical signs or symptoms of deterioration. The surgery involves opening the scar from the prior closure down to dura over the myelomeningocele. Sometimes the laminae are removed to obtain better exposure or to decompress the spinal cord. The dura is then opened, and the spinal cord and myelomeningocele are gently dissected away from the scarred attachments to the surrounding dura. Once the myelomeningocele is freed from all its scarred attachments, the dura and the wound are closed. The combined complication rate of this surgery is usually only 1-2% Complications include infection, bleeding, damage to the spinal cord or myelomeningocele, which may result in decreased muscle strength or bladder or bowel function. Many children require only one untethering procedure. However, since symptoms of tethering can occur during periods of growth, 10-20% will require repeated surgery.

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Tumors of the Central Nervous System Clinical Presentation Brain tumors present with 1. Progressive neurological deficits 2. Seizures 3. Nonfocal neurological deficits e.g. headache, dementia, personality change, gait Nonfocal disturbances can be also due to Raised ICP, hydrocephalus or diffuse tumor spread. Stroke like onset may suggest hemorrhage into tumor. Tumors may be large at presentation if located in a clinically silent region e.g. prefrontal of growing very slowly. Tumors in the diencephalic, temporal, frontal lobes may have personality changes. Systemic symptoms e.g. Malaise, fever, LOW/LOA may suggest metastatic disease. Evaluation: Neuroimaging with CT/MRI with contrast, CSF fluid for examination e.g. meningeal metastases. Symptomatic Treatment Glucocorticoids(Dexamethasone 12-20mg/day in divided doses e.g. 4-8mg tds) Prophylaxis with anticonvulsants e.g Phenytoin DVT prophylaxis e.g. TED stocking or low dose s/c enoxaparin Tumors in CNS account for up to 20% of cancers in childhood. 70 % of childhood CNS tumors occur in the posterior fossa 70% of CNS tumors in adults occur supratentorially Equal incidence of metastatic and primary CNS tumors in adults 1. 2. 3. 4. They are classified according to cell types:Gliomas Neuronal tumors Poorly differentiated tumors Lymphomas 5. 6. 7. 8. Germ cell tumors Meningiomas Nerve sheath tumors Metastatic tumors

Astrocytomas Fibrillary astrocytomas represent abt 80% of all brain tumors, occurring usually in the cerebral hemispheres. They can be well differentiated, anaplastic and aggressive (anaplastic astrocytomas) or extremely high grade( glioblastoma multiforme, GBM). Low grade tumors may remain static or grow slowly over years. GBM has poor prognosis, mean survival length is about 8 months. Treatment is difficult; infiltration along white matter pathways prevents total resection. Surgery is for tissue diagnosis and to control mass effect. RT prolongs survival and improves quality of life. Systemic Chemotherapy is marginally effective, used as an adjunct to RT for high grade tumors Other giomas
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Brainstem gliomas -These occur in 1st 2 decades of life, with 50% progressing to GBM at autopsy. After radiotherapy, 5-year survival is 20 to 40%. Pilocytic astrocytomas-These occur in children and young adults, usually in the cerebellum or floor of third ventricles. Often cystic, grows slowly and rarely infiltrative. Pleomorphic xanthoastrocytomas-These occur most commonly in the superficial temporal lobes, in children and young adults with history of seizures. Oligodendrogliomas 5-15% of gliomas. Most common in midlife, occurs the cerebral white matter and has better prognosis than patients with astrocytomas. They average about 5-10 years mean survival. Well circumscribed, often cystic with calcification (90%) and focal haemorrhages. Ependymoma These arise from the ependymal lining of the ventricles thus CSF dissemination is common. In 1st 2 decades, they occur in the fourth ventricle, later, spinal cord is the most common. Germinomas Tumors of midline brain structures. Onset in second decade. Uniformly enhancing mass on neuroimaging. Complete excision >85% 5-yr survival. Chemo and Radiosensitive. Primitive Neuro-Ectodermal tumors(PNET) 50% in the posterior fossa, derived form neural precursor cells. Treatment with surgery, Chemo and RT Primary CNS Lymphomas B cell; most common in immunosuppressed pts. May present as a single mass lesion( in immunocompetent pts) or as multiple mass lesions(in immunosuppressed). Silt lamp to exclude ocular involvement. Prognosis is poor. Dramatic transient response with steroids. Treat with RT and chemotherapy. Meningiomas Extra-axial mass attached to dura, dense and uniform contrast enhancement is diagnostic. Total resection of benign lesion is curative; subtotal excision with RT reduces recurrence < 10%. Small asymptomatic lesions can be followed up. Schwannomas Vestibular schwannomas present as progressive unexplained hearing loss. MRI reveals a dense uniformly enhancing tumor at cerebellopontine angle. Treatment is surgery.

Metastatic tumors of CNS


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Haematogenous spread is the most common. Skull mets rarely invade CNS. Most common metastasis to CNS Site of primary Brain Mets % Leptomeningeal mets % Lung 40 24 Breast 19 41 Melanoma 10 12 GIT 7 13 GUT 7 others 17 10 Spinal Cord compression 18 24 4 6 18 30

Brain metastases are well defined with MRI and enhance with gadolinium; triple dose contrast is most sensitive. Differential include abscess, radiation necrosis, granuloma, lymphomas, bleeds. CSF cytology is rarely helpful. 1/3 have unknown primary and 1/3 primary is never identified. Leptomeningeal Metastases Presents with headache, encephalopathy, cranial nerve or polyradicular symptoms. Diagnosis by CSF cytology, MRI (nodular deposits or diffuse meningeal enhancement). Associated with hydrocephalus. Aggressive treatment with intrathecal methotrexate or Focal external beam RT produces response in 20% of pts. Spinal Cord compression from metastases Most common from lung, breast and prostate. Back pain precedes motor and sensory deficits and incontinence. Medical emergency; early recognition is essential; diagnosis by MRI spine. Progression may be slowed by glucocorticoids while awaiting surgery or RT Management Screen for occult cancer, look for melanoma, Tumor markers(CEA,-FP,CA19-9, CA15-3),CT thorax, abd, pelvis. Additional investigations if necessary e.g. OGD, colonoscopy. Biopsy of accessible tumor is needed to plan treatment. Refer to Medical oncology. Treatment Initial treatment with dexamethasone, anticonvulsants prophylaxis. Whole brain RT (WBRT) is given as microscopic spread is likely. A single metastasis may be excised followed with WBRT. Systemic chemotherapy may have responses in some cases Radiation Therapy (RT) The goal of RT in treating tumors is to cause cell death or to stop cell replication. The photons impart energy to the cells by photoelectric effect, by Compton effect or by pair-production. The amount of energy is quantitated by 1 Gray (1 Joule/kg). Conventional External Beam RT

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Total radiation dose is delivered in a series of smaller brief applications, radiation injury is a function of dose, exposure time and area exposure. Following surgery for tumor, most surgeons wait 7-10 days before instituting RT to surgical site Germ cell tumors and lymphomas melt away with RT but tend to recurr later. Radiation necrosis may mimic recurrence or de novo tumor. MR Spectroscopy PET;SPECT- may be useful in differentiating. Manifestations of radiation effects 1. Decreased cognition e.g. dementia; lower IQ in children 2. Injury to anterior optic pathways 3. Injury to HPO-axis, growth retardation in children 4. 5. 6. 7. Primary hypothyroidism Malignant transformation Induction of new tumor leukoencephalopathy

Complications of Radiation Therapy 3 patterns of radiation injury after CNS RT 1. Acute Headache, sleepiness, worse neurological deficits during or immediately after RT. Usually self-limiting and glucocorticoids responsive 2. Early delayed Somnolence(esp. in children), Lhermittes sigh; within 4 months of RT. Increased T2 signal on MRI. Also self-limiting and responses to glucocorticoids 3. Late delayed Dementia or progressive neurologic deficits.; typically 1 year after RT. White matter abnormalities on MRI, ring-enhancing mass due to radiation necrosis. PET distinguishes delayed necrosis from tumor recurrence. Progressive radiation necrosis is best treated palliatively with surgery. Endocrine dysfunction due to hypothalamus or pituitary gland injury can be also delayed effects of RT Treatment Symptoms usually respond initially to steroids. Surgery has a role in recurrence and for mass effect. Tolerance of normal brain to RT is abt 65-75 Gy given over 6 to 8 weeks, in a 5 fractions/week e.g. 30 treatment over 6 weeks (RT necrosis abt 5%) Neuro-ophthalmology Cranial nerve palsies o Isolated: 3,4,6,7 o Multiple: Cavernous sinus syndrome, Cerebellopontine angle syndrome, lateral medullary syndrome Traumatic eye injuries A. Traumatic optic neuropathy C. Open globe injuries B. Blowout fracture D. Hyphaema Cranial nerve palsies May occur in isolation or in groups. If isolated, may be an ischemic event e.g. mononeuropathy secondary to diabetes. Ask for hx of DM, hypt, IHD, hyperlipidemia, smoking.

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Pattern of multiple cranial nerve palsies may give clue to location of lesion. Keep in mind that meningeal irritation, myasthenia gravis and Guillain-Barre syndrome may mimic multiple cranial nerve palsies. (A) Isolated CN palsies Oculomotor (third) nerve palsy History
Ptosis Diplopia Pain/ headache/ vomiting Ischemic risk factors DM, hypt, etc Tempo of symptoms acute onset, rapid progression? Symptoms suggestive of increased intracranial pressure

Examination
Ptosis partial/ complete Affected eye down and out Limited ocular movements except abduction ( CN6) and depression in adduction (CN4) Pupils Determine if palsy is complete or incomplete

Dilated pupils surgical third (nerve compression, esp. of outermost autonomic fibres) Pupil sparing medical third Isolated versus multiple CN

Other cranial nerves Investigations Surgical third Urgent MRI/ MRA Medical third BP, bld sugar

Delineate aneurysm/ tumour

Management
Cover affected eye to relieve diplopia Surgical third Intracranial aneurysm - clipping Tumour assess resectability Medical third Review early to ensure no evolving pupil involvement Refer neurology/ neuro-ophthalmology Conservative mx To treat as surgical third if pupil involved (see above) Gradual resolution of CN palsy over 3mth

Trochlear (fourth) nerve palsy History


Vertical diplopia Headache Trauma any LOC? Ischemic risk factors Superior oblique depresses, abducts and intorts the eye. Palsy causes the overaction of the elevators (inf oblique, sup rectus) Long intracranial course of 4th nerve makes it vulnerable to injury

Physical examination
Vertical squint Ocular movements Other CN involved? Affected eye may be slightly higher Limitation in depression in adducted position

Investigations
Neuroimaging CT/MRI BP, bld glucose Look for tumour, aneurysm (rare) Ischemic risk factors

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Management
Cover affected eye to relieve diplopia Conservative mx if ischemic Resolution in 3 mth

Abducens (sixth) nerve palsy History


Horizontal diplopia Headache, vomiting Trauma Hx of NPC, prev radiotherapy Ischemic risk factors Suggesting increased intracranial pressure

Physical examination
Ocular movements Unilateral or bilateral 6th palsy? Other CN involvement Neurological examination Fundoscopy optic disc Limitation in abduction of affected eye Bilateral: possible false localizing sign

Look for papilloedema ==> False localizing CN 6 palsy Look for intracranial lesion Ischemic risk factors

Investigations
Papilloedema and/or bilateral CN 6 palsies neuroimaging BP, bld glucose

Management
Cover affected eye to relieve diplopia Refer ENT Conservatie mx if ischmemic To assess for possible underlying NPC Resolution in 3mth

Facial nerve (seventh) palsy History


Facial asymmetry Inability to close eyes

Physical examination
Loss of forehead creases Unable to close eye Loss of nasolabial fold Drooping of angle of mouth Other CN involvement UMN lesion Neurological exam brainstem, cortical lesion LMN lesion: try to identify site Cerebellopontine angle Temporal bone Ear Parotid gland Bellss palsy LMN lesion (if preserved - UMN lesion) Risk of exposure keratopathy potentially sight threatening esp. if infected

CVA (isch/ haem), tumour CN 6,7,8 +/- 5 Fracture (hx of trauma, Battles sign, CSF otorrhoea) Otitis media, Ramsey-Hunt Tumour, trauma Diagnosis of exclusion

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Investigations Management
Protect the cornea tape lid shut at night, copious lubricants*, lateral tarsorraphy if exposure is severe Refer ENT

Neuroimaging Refer eye to assess exposure keratopathy Ear lesions

* Lubricants Eyedrops: Gutt hypromellose Q3H (cheap, easily available, single bottle but preservatives bad for corneal epithelium in long term) Gutt tears naturale free/ Refresh plus Q2H (preservative free, comes in disposable tubes better for eye in longer term, but more costly) Ointments: longer-lasting occ solcoseryl/ Duratears/ Vidisic TDS or QDS (B) Multiple cranial nerve palsies Cavernous sinus syndrome (CN 3,4,5,6) History, Physical Exam: Combination of the above-mentioned CN palsies Etiology: Vascular o aneurysm: intracavernous sinus carotid aneurysm, posterior cerebral artery aneurysm o cavernous sinus thrombosis Inflammatory o meningitis o bacterial: syphilis, TB o viral: herpes zoster o Tolusa Hunt Tumour o primary: pituitary adenoma, meningioma, cranipharyngioma o secondary: NPC, lymphoma, mets Trauma o Carotid-cavernous sinus fistula Cerebellopontine angle syndrome (CN 5,6,7,8) Etiology: Tumour o Acoustic neuroma o NPC o Clivus meningioma Trauma o Basal skull fracture

o Pontine glioma o V CN neuroma

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Lateral medullary syndrome (5,8,9,10) Etiology: Stroke Multiple sclerosis Clinical features: CN 5 and spinothalamic tract crossed hemihypoalgesia CN 8 nystagmus CN 9, 10 dysarthria, dysphagia Sympathetic Horners (ptosis, miosis, anhydrosis, enophthalmos) Cerebellum nystagmus, disdiadokinesia, intention tremor Traumatic Eye Injuries Blowout fracture Fracture of the orbital walls. Medial and inferior walls most commonly involved History
Mechanism of injury Diplopia, pain with ocular movement Physical Exam Enophthalmos Periorbital swelling Orbital rim tenderness, crepitus, step Blunt injury object larger than orbit

Signs suggestive of blowout fracture # of orbital wall. Maxillary haemoantrum

Investigations
XR orbits CT orbits

Management
Refer to plastics/ eye (oculoplastics) Pt to avoid blowing nose Oral antibiotic prophylaxis

Traumatic optic neuropathy


Damage to optic nerve: transaction, impingement by bony fragments, or compression by haemorrhage Blurring of vision after trauma History

Examination
RAPD Visual acuity Usually very poor but can be normal Bony impingement, transaction of optic n, retrobulbar haemorrhage Refer eye, KIV IV steroids

Investigations
CT orbits (fine cuts)

Management

Open globe injuries Can result from blunt trauma, (high velocity) foreign body entry. Pain and decreased vision may be elicited in history. Severe subconjunctival haemorrhage and limited extraocular motility are features that may be present grossly. Refer to eye specialist for assessment and primary repair. Hyphaema

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Blood in the anterior chamber of the eye. Layer of blood may be visible on general inspection. Ususally resolves spontaneously but may be complicated by increased intra-ocular pressure causing pain. Refer to eye specialist for assessment. Useful numbers SGH neuro-radiology reporting room 6326 6062 SNEC mainline 62277255 Neuro-ophthalmology consultants (SNEC): Prof Barry Cullen, Dr Sharon Tow

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Surgical procedures and operations Elective Neurosurgical admissions (Guidelines only) Most elective admissions will be for Brain Tumour patients as well as Spinal cases. CRANIOTOMY 1. History and examination 2. Check Relevant pre-op investigations are done, if not then order: FBC, U/E/Cr, PT/ PTT, GXM 2 to 4 units (aneurysm surgery will need at least 4 units). Trace all old notes. CXR / ECG as clinically appropriate If patient has been to Pre-admission Clinic then check all blood inv and CXR / ECG are with the case notes 3. Make sure CT / MRI +/- angiogram is present with the notes. Some patient will require specific MRI sequences called STEALTH. For these patients stereotactic markers will need to be placed on them(ALWAYS CHECK WITH REGISTRAR WITH REGARD TO POSITION IF IN DOUBT) if MRI needs to be done, call Radiologist or MRI counter and fax the request form with the urgent form to the MRI counter. Write on form for STEALTH MRI Brain. Please exclude Contraindications to MRI ! Place the markers, insert IV cannula and then send the patient down. If the markers are to come off then they need to be replaced at the exact spot. MRI will burn a disc for STEALTH patients. This must accompany the patient to theatre .Check consent has been signed and side specified; Write and dispatch OT chit. 4. All patients will require an IV drip when NBM. 5. Consultants may request specific orders on the admission form check that these have been done or ordered. Aspirin should have been ceased for 1 week prior to surgery.

SPINAL CASES 1. History and examination check for pain, document pre-op neurological deficits 2. Pre-op investigations: FBC, U/E/Cr, PT/PTT, GXM 1 unit; CXR / ECG as clinically appropriate 3. Check CT / MRI / SPINAL x-rays available pre-op 4. Consent signed and levels specified; Write and dispatch OT chit 5. Special orders: Some patients will require C- collars to go with patient to surgery. Some consultants prefer pre-op skin markers (paper clips stuck to skin by micropore tape) to be placed at the relevant spinal levels and X-rays to be done with the skin markers. This is to facilitate intraop planning. CAROTID ENDARTERECTOMY 1. History and examination

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Blood pressure control is imperative pre-op. If patient is markedly hypertensive then inform registrar ASAP as medications may need to be altered. 2. Pre-op Investigations: FBC, U/E/Cr, PT/PTT, GXM at least 4 units CXR / ECG as clinically appropriate 3. Check Carotid angiogram is done, if not then see if it has been organised . 4. Check consultants specific orders aspirin does not need to be stopped pre-operatively but check with consultant / registrar if not sure. 5. If patient is on continuous heparin infusion then check with your consultant when to cease preop. There is a protocol in the wards for the management of heparin infusion please read it before starting heparin for anyone. 6. Check consent signed and side specified. 7. Write and dispatch OT chit 8. NBM at midnight with IV drip order TRANSPHENOIDAL PITUITARY SURGERY( see Clinical Pathway for details) 1. History and examination Document visual fields and visual acuity with Snellen chart if no pre-op eye review requested Make sure no signs or symptoms of sinusitis (if present then contact registrar) 2. Pre-op investigations FBC, U/E/Cr, PT/PTT, GXM 2 units ECG / CXR as clinically appropriate Make sure pituitary hormone work up results is in case notes. 3. Check CT / MRI films are present 4. Pre-op consults: See if pre-op consult for ophthalmology or endocrine required. If unsure then check admission notes, clinic notes or with consultant in charge. 5. Medications may need to be charted pre-op as requested by consultant or endocrinology, check for these in the notes and order them as necessary 6. Check consent signed 7. Write and dispatch OT chit 8. NBM at 12 midnight with IV drip order

EMBOLISATION / ANGIOGRAM 1. History and examination 2. Pre-op Investigation: Angiogram: requires FBC, PT / PTT, Urea and Cr Embolisation (done under GA): FBC, U/E/Cr, PT/PTT, GXM 2 units, CXR and ECG as appropriate 3. Consent for angiogram to be taken by MO in charge see attached sheet on consent. Consent for Embolisation will be taken by neuroradiologist and will be with the request form usually in angio suite already. 4. NBM at midnight with IV drip for all patients.

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Craniotomy and its complications Craniotomy is an operation where a window is cut into the skull bone to allow the surgeon to operate on the brain. The purpose of the operation may be to remove a blood clot, tumour, or blood vessel disorder among others. Modern advances have made brain surgery safer. However, as with all surgical procedures, complications can occur. Some of these risks and complications are inherent in any operative procedure, especially when general anaesthesia is administered. In addition, some of the possible complications specifically following Craniotomy are: Cerebral haemorrhage This may occur at the site of operation usually some time after the operation is completed. If haemorrhage is suspected, it can be confirmed by CT brain scan. If the haemorrhage is large, further surgical procedures may be required to treat it. It may result in irreversible paralysis, coma or even death. Post-operative brain swelling This can result from manipulation of the brain. It may require the original bone window to be left out when the skin incision is closed (this will require a second operation to replace the bone window at a later time). Further surgery may be required to treat the swelling. Post-operative infection This is a potentially very serious complication that occurs despite the routine surgical prophylaxis against infection. Treatment of infection can involve multiple surgical procedures and prolonged hospital stay for antibiotic treatment. Post-operative brain water circulation disorder This is due to disturbance of the brain water circulation pathways that sometimes develops after surgery. Its treatment may require further surgery to allow diversion of the brain water to another body cavity. This can sometimes have permanent effects (neurologic deficit) Post-operative brain malfunction (neurologic deficit) The likelihood of this complication varies from one operation to another. It may be a temporary condition or it may be permanent. It may be the end-result of other complications (eg. haemorrhage, swelling, infection). The patient may experience the loss of vision, hearing, speech/ language ability, sensation, paralysis of limbs, loss of coordination of limbs or cognition (thinking ability), specific cranial nerve dysfunction, coma or even death. Seizures This develops in some patients after surgery. The patient may be required to take anti-convulsant medication for life.

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Frameless Stereotactic Neurosurgery The first part of the procedure involves CT or MRI performed with fiducial markers which are taped to the scalp before the brain is imaged. Frameless systems can also use bony landmarks e.g. mastoid process. The second part utilizes a set of guides orientated to the same coordinate system registered in the computer containing the brain images. Once registration is completed, the computer can show the relationship of our surgical instruments to the imaged brain. Frameless or image guided surgery is very helpful for the accurate approach and removal of large brain tumors Indications: 1. Biopsy deeply structures esp. in near eloquent brain, brainstem lesions, small lesions, pts unable to tolerate GA for open biopsy. 2. Catheter placement drainage of deep lesions, EVD, indwelling catheter for intratumoral chemo, radioactive implantation. 3. Electrodes placement Deep Brain stimulation electrodes, epilepsy electrodes 4. Evacuation of ICH using adjunctive urokinase 5. Localising lesion for open craniotomy 6. Stereostatic radiosurgery Steps: 1. MRI/CT Scan is done usually the day before the operation. 2. Place fiducial markers on the patients to act as reference points. 3. Some small areas of shaving may be needed for the markers to stick. 4. Use permanent marker pen to mark the location. 5.Place at least 8 fiducials, with 1-2 on contralateral side, on the bony attachment of the head which are not movable e.g. mastoid process. Some markers should be higher, lower and at the level of the brain tumour. A wide area needs to be covered. But the location of the fiducial markers should be accessible by the surgeon during the actual positioning of the patient intraop (if the patient is supine, it will be useless to have markers on the occipital protuberance as it is not accessible intra-op) 6. If unsure of the location of the markers, consult the registrar or neurosurgeon for the exact placement if in doubt before scan. 7. Advise pt and nurses not to wash hair and try to keep the fiducial markers in place till operation External Ventricular Drain(EVD) These drains are catheters placed for several different reasons including acute obstructive hydrocephalus (eg. from a blood clot in the fourth ventricle), tumor obstructing the aqueduct or for communicating hydrocephalus such as after a SAH or meningitis. They are also placed temporarily after removing an infected VP shunt while the infection is treated with antibiotics prior to replacing another VP shunt. The nurse will be checking the drain and taking measurements. A sample of CSF may be taken. There will be CSF in the drainage system. The fluid may be clear, yellowish, or bloody.

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The patients GCS level should be monitored closely after any adjustment to the height of the EVD, clamping, removal etc. EVD Removal 1. To be done under aseptic condition 2. The stitch holding the drain will be removed. The drain is removed. 3. ALL EVD drain tips should be sent for culture. (All EVD drain culture results should be traced before sending the patient home) 4. A stitch will be used to close the drain exit site. 5. A small dressing will be placed over the area. The Neurosurgeon in charge will decide on the duration of EVD drainage before weaning, change of EVD or conversion to a VP shunt. In general, EVD catheters are changed after 7 days or earlier if there is signs of infection. These drains are subject to 3 main problems: 1. Infection
2. Dislocation (usually during a turn or when pulled by a patient)

3.

Blockage (usually due to blood clots)

In general the EVD drainage is regulated by gravity. The EVD drip chamber is usually set at 510cm above the external auditory meatus (= level of foramen of Monroe) and left to free drainage. This height can be adjusted to achieve more drainage (by lowering it) or less (by raising it) according to the clinical situation. Physiological Facts 1) Average daily CSF production = 300ml/day 2) Average Lateral Ventricle volume = 20ml CSF 3) Average Total CSF volume = 150ml

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1. 2. 3. 4.

Management of a Blocked CSF drain. Note the clinical situation. If there is no neurologic deterioration or change, then discuss with the neurosurgeon regarding flushing. He may opt to observe the patient. If CSF drainage is mandatory an attempt to flush the catheter will be ordered. Use aseptic technique and wear a sterile gown Dead space of EVD catheter = 2ml established can repeat up to 2 more attempts. If there is still no flow, inform the neurosurgeon. He may decide to replace the catheter.

Use 2ml of sterile N/S to flush the catheter from the 3-way tap point. If no flow

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Ventriculo-peritoneal shunt The Operation After a general anesthetic is administered, the patient is positioned on his back, with his head turned to one side. The hair over the scalp incision area is shaved. Usually two incisions are made: a small incision in the abdomen and a curved incision in the scalp. The scalp flap is then turned back to expose the skull, into which a small burr hole is drilled. This uncovers the dura, the brain's covering, over the enlarged ventricles. The shunt is inserted first into the abdominal incision and is brought beneath the skin over the abdomen, chest, and neck, into the scalp opening. After the tubing and reservoir are in place, a small cut is made in the dura and a ventricular tube is inserted into the brain's right ventricle. The reservoir is then attached to the ventricular tube and is fitted into the opening in the patient's skull. Signs of a shunt infection 1. A fever that is equal to or higher than 38.5 C 2. Redness and tenderness along the path of the VP shunt 3. Swelling along the path of the VP shunt 4. Meningitis and Kernigs sign 5. Change in mental state

Ommaya Reservior Cerebrospinal fluid (CSF) surrounds the brain and spinal cord. Sometimes, medications need to be given into the CSF because intravenous medications will not reach that area. Medications can be given into the CSF when an ommaya reservoir is inserted. The ommaya reservoir, or port, is a dome like device that is placed surgically under the scalp. It is used for: 1. Give medications directly into the CSF 2. Measure the pressure of the CSF 3. Take samples of CSF to be tested 4. Inserted into cysts for intermittent decompression SAMPLING AND DRUG ADMINISTRATION Consistent guidelines for access, injection of medications, and withdrawing CSF from the Ommaya reservoir will prevent infection or adverse outcomes. 1. All medications will be preservative-free. No alcohol or alcohol containing products should ever be used for site preparation of an Ommaya Reservoir. Maintaining sterile technique, prepare skin over Ommaya reservoir. Swab to cleanse skin over reservoir with povidone-iodine using a circular motion from inner to out. Repeat with two additional swabs. Allow to dry two minutes, then remove excess povidone-iodine with dry sterile gauze. 2. Insert needle (Need to use fine bore butterfly needle) through middle of dome, at an angle perpendicular to the dome. Gently advance needle until the tip of the needle meets the backstop of the reservoir. (Alternate insertion sites in dome.) 3. If lab studies on CSF needed, withdraw 2 ml CSF, clamp tubing, and discard CSF. Then withdraw 1-4 ml. 4. Inject medication slowly (3-5 minutes) into reservoir 5. Remove scalp vein needle from reservoir. 6. Place sterile 2 x 2 dressing over reservoir. 7. Maintain pressure at injection site 3-5 minutes. 8. If need for multiple aspirations use the 4 quadrant technique. 9. Observe patient throughout the procedure. Stop the aspiration if patient complains of headache, giddiness, nausea, vomiting or new neurological findings. 10. When instilling medications use isovolumetric technique. E.g. aspirate 2ml, instill 1ml medication, flush with 1ml normal saline/aspirate. (Dead space of ommaya reservoir =1ml)

Lumbar Puncture Indications: 1. To obtain CSF sample to check for meningitis / cytology / immune markers / xanthochromia in subarachnoid haemorrhage 2. To measure opening and closing pressures via manometer especially in deciding for surgery in normal pressure hydrocephalus (NPH) 3. Therapeutic removal of CSF to assess for benefit of Ventriculo-peritoneal shunt in NPH. Contra-indications: 1. Raised intracranial pressure e.g. if non-communicating hydrocephalus, papilledema on ophthalmoscopy. All patients will require CT head prior to LP to reduce risk of coning is suspicion of increased pressure. 2. Cardiorespiratory unstable patients 3. Infection at the site of Lumbar puncture e.g. pressure ulcer 4. Coagulopathy Materials (will be prepared by nurses) Lumbar Puncture set with sterile gloves. Wear a mask and protective gown as well! Spinal Needle use a 20 / 22-gauge always if possible Manometer to measure pressure Sterile drapes Local Anaesthetic usually 5mls is sufficient Material for skin sterilization iodine and alcohol usually Adhesive pressure dressing Technique 1. Place the patient in the lateral decubitus position lying on the edge of the bed and facing away from operator. Place the patient in a knee-chest position with the neck flexed. The patient's head should rest on a pillow, so that the entire cranio-spinal axis is parallel to the bed. Sitting position is the second choice because there may be a greater risk of herniation and CSF pressure cannot be measured 2. Find the posterior iliac crest and palpate the L4 spinous process, and mark the spot with a fingernail. Prepare the skin by starting at the puncture site and working outward in concentric circles. Put on sterile gloves. Drape the patient. 3. Anaesthetize the skin and then insert in the midline with the needle parallel to the floor and the point directed toward the patient's umbilicus to anaesthetize between the spinous processes. 4. Next use the Spinal 22 G needle and advance slowly, in the same direction, about 2 cm or until a give is felt (piercing the membrane of the dura and entry into subarachnoid space). Then withdraw the stylet in every 2- to 3-mm advance of the needle to check for CSF return. If the needle meets the bone or if blood returns (hitting the venous plexus anterior to the spinal canal), withdraw to the skin and redirect the needle. If CSF return cannot be obtained, try one disc space up. 5. When cerebrospinal fluid begins to flow from the needle, discard the first few drops. Never aspirate CSF!!! 6. Measure the opening pressure with a manometer; allow the patient to relax, and check for good respiratory variation of the fluid level in the manometer to ensure that the needle is properly positioned.

7.

8. 9.

Remove the manometer and allow 1 to 2 cc of CSF to flow into each of the three sterile tubes. Send the first for glucose and protein, the second for Gram stain and culture and sensitivity (C&S), and the third for cell count and differential. A fourth tube, when indicated, is collected for viral titre or cultures, India ink preparation, Cryptococcus antigen, VDRL, or cytology (if needed). In subarachnoid haemorrhage, 3 tubes need to be collected to measure the differential cell count from bottle 1 to 3 as well as for xanthochromia. Measure the closing pressure obtaining CSF for investigations. Withdraw the needle without replacing the stylet. Dress the puncture site with a pressure bandage. Have the patient lie in bed for at least 6 hours and monitor parameters hourly for 6 hours. Document the procedure in the case notes.

Complications 1. Post-lumbar puncture headache: 2. Occurs in 10% to 30% of patients within 1 to 3 days and lasts 2 to 7 days. Lying flat relieves the pain. Treatment consists of bed rest and fluid with simple analgesics. 3. Can be reduced by using the most practical size needle that is 22 G. 4. Keep bevel of needle facing upward i.e. in the direction of the dural fibres.

Lumbar Drain These drains are catheters placed at the bedside into the lumbar subarachnoid space to remove CSF. Indications of Lumbar drain 1. Non-obstructive hydrocephalus (e.g. following SAH) 2. To treat CSF leaks resulting from cranial surgery or trauma The lumbar drain is a small plastic catheter used to remove CSF. It is inserted using the same technique as a lumbar puncture except in this case a Tuohy needle is used. The usual orders are to remove 100mls CSF per nursing shift. (300mls/day). Please check with the neurosurgeon in charge. The nurse will also be checking the drainage system frequently. The fluid may be clear or coloured. The head of the bed may be elevated. However, if the patient is going to sit up or assume the upright posture the drain must be clamped to prevent sudden over drainage and possible subdural hematoma. The risks of a lumbar drain are: - Meningitis - Hematoma - Bleeding - Leakage of cerebrospinal fluid (CSF) - Paralysis - Infection Lumbar drains are removed after about 1 week in this center. (Please check with the neurosurgeon in charge of the patient before removing the drains) Procedure 1. A standard LP is performed (See Steps 1-8 on Lumbar Puncture) 2. When CSF is encountered, the curve of the needle is directed superiorly, the stylet is removed, and the catheter is advanced into the subarachnoid space at least 20 cm (Fig. A). The catheter (17- or 18-gauge) is then slowly advanced with one hand, and the needle is simultaneously removed. 3. A local anesthetic agent is injected subcutaneously along the desired path of tunneling for the length of the needle. The free Tuohy needle(Fig. B) is passed from this direct lateral position and brought out through the initial LP site, with care being taken not to cut the catheter with the tip of the needle

Transsphenoidal Pituitary Clinical Pathway Pre-Op/Day of admission 1. Blds : FBC,U/E/CR, PT/PTT, Hep B, GXM 1 unit 2. Pituitary Hormonal profile if not done previously a. Synacthen test, fT4,TSH,GH,IGF1, FSH,LH,Testosterone,E2 3. ECG,CXR if more than 40 yrs or otherwise indicated 4. Diet of choice or Specific Diet( e.g. low salt, low fat, DM); NBM 12MN 5. Pre-op assessment by Endocrinologist, Ophthalmologists, Anesthetists if already not done before; Inform Endocrinologist of patient admission. 6. Order in IMR IV Cefazolin 2g and IV Metronidazole 500mg on call to OT; if pt allergic to beta-lactams, order IV clindamycin 600mg and IV gentamicin 1.5mg/Kg 7. IV hydrocortisone 100mg on call to OT. Day of Surgery/ 0 POD / Post-Op 1. CLC and parameters hrly, Hrly urine output and I/O charting; Visual charting 2. IF Diabetes insipidus/ Urine output >200mls/hr for 2 hrs a. Repeat Na+ and serum osmolality; Hypocount 6hrly 3. Assess for CSF leak and bleeding from nose a. Document total no. of nasal bolsters change requireed b. inform Neurosurgeon if excessive 4. IV hydrocortisone 100mg 8H unless Cushings a. If Cushings/Apoplexy/ Pre-existing Hypocortisolism i. continue IV hydrocortisone 100mg 6H b. If Pre-existing DI- administer s/c DDVAP 4g bd, nasal DDVAP can be started once nasal packs removed 5. Rest in bed, head up 30 degrees. Keep Urine catheter 1st POD 1. CLC and parameters hrly, Hrly urine output and I/O charting; Visual charting 2. IF Diabetes insipidus/ Urine output >200mls/hr for 2 hrs a. Repeat Na+ and serum osmolality; Hypocount 6hrly 3. Assess for CSF leak and bleeding from nose a. Document total no. of nasal bolsters change requireed b. inform Neurosurgeon if excessive c. Remove nasal pack if no bleeding 4. IV hydrocortisone 50mg 8H unless Cushings(8am,2pm,8pm) a. If Cushings/Apoplexy/ Pre-existing Hypocortisolism i. continue IV hydrocortisone 100mg 6H till last dose on 2POD 8pm ii. Can covert to Oral on 2POD if taking diet well b. If Pre-existing DI- administer s/c DDVAP 4g bd, nasal DDVAP can be started once nasal packs removed 5. If DI suspected- Inform Endocrinologist a. monitor I/O, hrly urine output; replace urine loss with 5% Dextrose b. monitor hypocount 6H.

6. Feeds to Diet as tolerated; Ambulate as tolerated 2nd POD 1. Review CLC, Visual charting and Monitor I/O, H/C 2. Assess for signs of Cushings- anorexia, N+V, myaglia, low grade fever a. Call Endocrinologist if signs presents 3. Remove IV plug, except for pts with Cushings disease 4. Remove urinary catheter if no DI or as ordered 5. Pts with intact cortisol axis(i.e. peak synacthen response>550nmol/l and 2nd POD cortisol> 450nmol/l) a. Stop hydrocortisone replacement 6. Pts with possible hypocortisolism(2nd POD<450nmol/l) a. Start hydrocortisone 20mg OM and 10mg ON 7. If Cushings disease(ACTH-producing adenoma) and 8am cortisol>50nmol/l) a. Continue IV hydrocortisone 100mg 6H 8. If pre-existing hypocortisolism a. Start oral hydrocortisone 40mg OM, 20mg ON 9. If Apoplexy a. Give at least double physiological dose; consult Endocrinologist 10. If pre-existing DI a. Nasal ddavp may be restarted once nasal packs are removed 11. Diet as order and tolerated: ambulate as tolerated 3rd POD 1. If pt well, no DI/fever/bleeding consider discharge 2. Assess as mentioned in 1st and 2nd POD 12. Pts with intact cortisol axis(i.e. peak synacthen response>550nmol/l and 2nd ,3rd POD cortisol> 450nmol/l) a. Stop hydrocortisone replacement 13. Pts with possible hypocortisolism(2nd ,3rd POD cortisol <450nmol/l) a. Start hydrocortisone 20mg OM and 10mg ON 14. If Cushings disease a. If deemed cured, oral hydrocortisone to be started; consult endocrinologist for dosage. b. If not cured, consult neurosurgeon, consider re-look surgery. 15. If pre-existing hypocortisolism a. Start oral hydrocortisone 40mg OM, 20mg ON 16. If pre-existing DI a. Nasal ddavp may be restarted once nasal packs are removed 17. Diet as order and tolerated: ambulate as tolerated 18. Obtain TCU Appointments and ensure medications cover till Endocrine TCU a. ENT 1 week b. Neurosurgeon 2 weeks, sodium on arrival c. Ophthalmologist 4 weeks for visual field assessment d. Endocrinologist 2 weeks for hormonal assessment, if Cushings or apoplexy, TCU 1 week. 19. Discharge advice to be reinforced

Stereotactic Radiosurgery Stereotactic radiosurgery uses 3-D computerized imaging to precisely target a narrow x-ray beam and deliver a high concentrated dose of radiation to the affected area. Staged radiosurgery, also known as fractionated stereotactic radiosurgery (FSR), is a process in which the total dose of stereotactic radiation is divided into several smaller doses of radiation, on separate days of treatment. Typically, this consists of two to five treatments. In some cases, staged treatment effectively kills the tumor while seemingly decreasing potential side effects compared with single dose radiosurgery. Treatment Uses Patients can receive stereotactic radiosurgery in addition to whole brain radiation. This technology allows high doses of radiation to be delivered to the tumor with minimal exposure to surrounding healthy tissue. Stereotactic radiosurgery is a noninvasive treatment option for patients arteriovenous malformations (AVMs), arteriovenous fistulas (AVFs), brain tumors, and trigeminal neuralgia. Arteriovenous Malformations (AVMs) and Arteriovenous Fistulas (AVFs) AVMs can occur anywhere in the body, but brain AVMs present substantial risks when they bleed. Dural AVMs occur in the covering of the brain, and are an acquired disorder that may be triggered by an injury. An AVF causes a disruption of normal blood flow patterns. It may be congenitla or acqiured e.g. injury Stereotactic radiosurgery targets concentrated radiation to the malformed vessels of the brain, which causes the abnormal vessels to close off. Unfortunately, this treatment is usually limited to lesions less than 3.5 cm in diameter, and may take up to two years to completely obliterate the lesion. Intracranial Tumors Stereotactic radiosurgery may be a treatment option for select patients with primary brain tumors such as acoustic neuromas, anaplatic astrocytomas, chordomas, craniopharyngiomas, glioblastomas, gliomas, hemangioblastomas, meningiomas, pineal tumors, pituitary adenomas, and some metastatic brain tumors that arise from other parts of the body, such as the lungs. It works in the same way as other forms of radiation treatment. The tumor is not removed, but radiation distorts the DNA of the tumor cells. As a result, these cells lose their ability to reproduce. Following treatment, benign tumors may shrink over a period of 18 months to two years. Malignant and metastatic tumors may shrink more rapidly, sometimes within a couple of months. Trigeminal Neuralgia Trigeminal neuralgia or tic douloureux is sometimes described as the most excruciating pain known to humanity. The pain typically involves the lower face and jaw, although sometimes it affects the area around the nose and above the eye. This intense, stabbing, electric shock-like pain is caused by irritation of the trigeminal nerve, which sends branches to the forehead, cheek, and lower jaw. It is usually limited to one side of the face.

Stereotactic radiosurgery delivers a single highly concentrated dose of ionizing radiation to a small, precise target at the trigeminal nerve root. Over a period of time and as a result of radiation exposure, the slow formation of a lesion in the nerve interrupts transmission of pain signals to the brain. Other Indications At some centers, patients who have Parkinson's disease, epilepsy or some form of psychoneurosis, such as obsessive compulsive disorder, may be treated on an experimental basis with stereotactic radiosurgery. More recently, with the advent of frameless techniques, stereotactic radiosurgery is being used for spine lesions; more frequently metastatic lesions, and less often, benign spine tumors. Types of Stereotactic Radiosurgery Gamma Knife After a stereotactic frame is attached to the patient's head using pins, computed tomography (CT or CAT scan) and magnetic resonance imaging (MRI) are taken of the brain to determine the precise location of the tumor. If the patient has an AVM, an angiogram and CT scan are performed with the frame attached. The Gamma Knife consists of a sphere containing 201 Cobolt-60 sources. These sources are positioned so that the beams are targeted to a point within a cavity in the instrument where the patient's head is placed and covered by a helmet which narrows the beams and shields the head from unwanted radiation. The radiation is controlled by the percentage of the 201 ports that are used, the number of exposures and the head position. Computer-guided dosimetry is specified to match the lesion. Different beam sizes are available by using different helmets with holes of various sizes. Lesions from 5 to 40 millimeters can be treated. By performing multiple exposures and by readjusting the helmet and head position, different lesion shapes can be achieved. This procedure takes approximately 30 minutes. Linear Accelerator (LINAC) After a stereotactic frame is attached to the patient's head by pins, computed tomography (CT or CAT scan) and magnetic resonance imaging (MRI) are taken of the brain to determine the precise location of the tumor. If the patient has an AVM, an angiogram and CT scan are performed with the frame attached. Computer-guided dosimetry is specified to match the lesion. Lesions up to 3.5 centimeters in diameter can be treated. A cone that approximates the size of the lesion is placed in the collimator of the linear accelerator. Cones range in size from 12.5 mm to 40 mm. The patient is placed lying on his or her back on the treatment couch of the linear accelerator. The head is secured to prevent movement while receiving treatment. Radiation is targeted at the lesion from different directions called arcs. A predetermined amount of radiation is delivered in an arc and then the treatment couch is rotated along with the collimator housing the cone. This sequence continues until the therapy is complete. The number of arcs used varies from at least four to six and takes approximately 30 minutes. Some devices, like the CyberKnife, do not use frames, but masks to hold the head in place. Multiple manufacturers make this type of machine, which have brand names such as Peacock, XKnife, CyberKnife, Clinac, etc. Benefits

Surgical risks such as infection are not an issue, and there is little discomfort. Patients may be lightly sedated but are awake throughout the procedure. Hospitalization is short and at most, requires an overnight stay. The majority of patients are treated on an outpatient basis. As a result, patients have less discomfort and much shorter recovery periods. Recovery Following stereotactic radiosurgery, bandages are usually placed over the pin sites from the stereotactic frame, which should be removed the following day. Patients may be observed for a specified time after the treatment before they go home, or they may be kept in the hospital overnight for observation. Some people experience minimal tenderness around the pin sites. Most can return to their usual activities the following day if swelling is not bothersome. Follow-up The neurosurgeon will want to see the patient in the clinic about one month after the procedure. A neurological examination will be performed. Often, a diagnostic test such as a CT scan or MRI will be performed about six months after the procedure to check on the status of the radiated area. These changes may take from one to three years to take effect.

Neurosurgical Trauma Management Triage - mild head injury GCS 15-13 - moderate head injuryGCS 12-9 - severe head injury GCS 8-3 Mild head injury - History - place worksite, RTA, Home etc. - mechanism fall, assault etc. - ? alcohol use - pre existing medical problems - drugs esp antiplatelets, anticoagulants, anticonvulsants. Exam - Basic + complete neurologic exam - Basic general exam - Document all external injuries and chart on diagram - Document & chart all other identified non-head injuries - Document status of cervical spine exam - Clinical exam if asymptomatic for neck pain. - If symptomatic, ie., supplement with x-rays (AP, lat, open mouth), flex/extension views if necessary If you identify spinal tenderness or significant restriction of ROM or neurologic exam showing deficits in limbs, then treat as potential cervical spine injury until cleared by consultant (ie., spinal nursing and hard collar). - If upper limb paresis with absent/weak reflexes a/w head injury (esp motorcycle injury) look for brachial plexus pattern of deficit or central cord syndrome. CT scan - document lesions seen - site - size (for contusions) - assess for vault and skull base fracture. Investigations - FBC, U/E, PT/PTT, GXM (if CT scan +ve for Hemorrhage or #) CXR, ECG (if CT scan +ve as above). Management Acutely - Mx in GW - Hourly CLC, NBM for 24 hr - Correct any coaglopathy. Stop all anticoagulant and antiplatelet medications - Consult neurosurgeon re: need for phenytoin prophylaxis if lesion seen on CT (apart from isolated skull #)

Later - Discharge if alert, well and self caring. - Physiotx, MSW referral as appropriate. - if skull base # present assess for CSF leak, cranial nerve injury. - consult neurosurgeon re: plans to restart anticoagulant and antiplatelet medications when appropriate. Moderate Head Injury Same as for mild head injury. In addition: assess for evidence of raised ICP Signs: unequal pupils Severe headache, vomiting >2x BP >200 mmHg Bradycardial <70 bpm. CT: EDH, SDH, ICH, SAH Cerebral edema - gray/white interface blurred Obliteration of perimesencephalic spaces Midline shift, uncal herniation. Management ICA kiv ICU. Document cervical spine status. Consult neurosurgeon re: - use of mannitol - use of anticonvulsant prophylaxis - need for op If no initial plan for op: - if GCS worsens by 2 points or more transfer to ICU and/or prepare to intubate. Consult neurosurgeon on call re-need for CT, need for op. - intubate with anesthesia supervision if you do not have extensive experience in the procedure. - initiate mannitol therapy or additional bolus if already on mannitol. Treat infection as appropriate DVT prophylaxis TED stockings. - Assess by physiotx, speech tx, MSW as appropriate. - Discharge to home, TTSH TBI unit, nursing home as appropriate.

Severe Head Injury Triage - isolated head injury ) In both cases - polytrauma ) Main priority: Airway Breathing Circulation Physiological Isolated Head Injury comparison: Blood pressure Normal to high BP can be be low from blood loss due to : - severe (unattended) scalp laceration direct external bleeding from major dural sinus injury. - Extensive skull base or facial #. (may be occult and seen only on N/G tube aspiration) Normal to low (Cushings response) Head up 30 (BP normal) Appropriate ( if BP Normal) Aim for PCO2 ~ 35 mmHg

Polytrauma Normal to Low

Pulse rate Ideal posture Hyperventilation

Normal to High (BP low) - Supine or legs raised if appropriate Inappropriate(if SBP is < 90mmHg) CPP compromised by low systemic perfusion pressure. Further cerebral vasoconstriction not helpful. Aim for PCO2 40 mmHg Inappropriate( if SBP is < 90 mmHg ) Low BP - Further diuresis will result in further volume loss. Inappropriate until hemodynamically stable (or as decided by Trauma Surgeon) Common

Mannitol

Appropriate ( if BP Normal) 100ml of 20% solution stat + 6 hrly Appropriate (BP stable)

CT scan

Coagulopathy

Common

Management - in NICU follow NICU protocol - may be non-operation or operation as decided by neurosurgeon. - in general - treated with mannitol (omitted if hypotensive) - treated with prophylactic anticonvulsants - treated with mild hyperventilation (unless hypotensive)
ICP monitoring used as decided by neurosurgeon.

tracheostomy as decided by neurosurgeon/intensivist treat pyrexia, infection correct coagulopathy rapidly.

Use of IV Mannitol - must have indwelling urethral catheter & contraindicated if unable to catheterise. (risk of intraabdominal bladder rupture). If necessary consider suprapubic catheterisation. - to be avoided - if patient has ESRF (patient unable to produce urine and this will lead to pulmonary edema). - if patient is in heart failure (it can acutely raise intravascular volume and worsen the failure). - to be done with I/O balance charting - to be done with regular monitoring U/E/Cr. Use of prophylactic anticonvulsants in the absence of established seizures, used in situations of raised ICP (because seizures will worsen ICP further) - if no raised ICP, used in situations considered at high risk for precipitating seizures. - in general used for the first week post-trauma - consult neurosurgeon re: initiation and withdrawal of therapy. - generally not used for chronic subdural haematomas, basal ganglia haemorrhages, cerebellar, brainstem lesion. Use of prophylactic antibiotics for skull base fracture with/without CSF leak - proven by multiple RCT to be of no use in preventing meningitis in skull base fracture with or without established CSF leak.

Protocol for Management of Severe Head Injuries in the Neuroscience ICU


Aim: To standardize the monitoring and management of patients with severe head injuries (SHI) admitted to the Neuro-intensive Care Unit (NICU), focused on preventing secondary insults to the brain and thereby improving patient outcome. Inclusion Criteria: 1. SHI with post-resuscitation GCS 8 admitted to NICU. 2. Moderate HI with GCS >8, admitted to the NICU for close monitoring due to high risk for deterioration. 3. Post-craniotomy (for mass lesions) with brain swelling or potential for further brain swelling. 4. Intra-cranial mass lesions with potential for further swelling and deterioration.

Exclusion Criteria: 1. SHI with intractable hypotension despite maximal resuscitation and assessed to be unlikely to survive. 2. Patients with clinical and compatible CT evidence of brainstem death. 3. Presence of a terminal illness for which active management of the SHI is deemed futile.

Admission and Transfer All patients admitted to NICU from the Emergency Department (ED), general ward (GW) or through inter-hospital transfer, must first be triaged and accepted by the neurosurgical registrar on call. The procedure for accepting of new cases from ED and the movement protocol from ED to the scan room and then to NICU is covered under a separate protocol.

Initial Assessment and Management Resuscitate aggressively and promptly to correct any hypotension and/or hypoxemia, which are important causes of secondary brain injuries. The AIRWAY, BREATHING and CIRCULATION must be assessed IMMEDIATELY upon admission. All SHI with GCS 8 should be intubated, if not already intubated in the ED, to protect the

airway and assure effective ventilation and oxygenation. Patients for transfer to the NICU from GW should be intubated first prior to transfer. Aim to keep MAP 80 mmHg and SpO2 >95%. Patients with isolated closed head injuries should NEVER be hypotensive, unless already brain dead. If hypotensive, always SUSPECT AND LOOK FOR other causes e.g. intra-abdominal bleeding, scalp wounds, base of skull fractures, thoracic injuries or pelvic fractures. ALL SHI patients should have a cervical collar to protect the cervical spine till the neurosurgeon-in-charge has cleared the neck after reviewing the cervical spine x-rays CT scan. In patients expected to require the cervical collar for <7 hrs, a reusable stiff collar may be used. In all other cases, ask for the Aspen collar.

Patient Monitoring Standard hemodynamic monitoring for ALL SHI patients: o Continuous ECG, pulse oximetry, core temperature (rectal) o Automated oscillometric NIBP (cycle q 30 min; if no IA line inserted, cycle q10-15 min) o Arterial and CVP lines o Hourly urine output and I/O fluid balance Standard neurological monitoring for ALL patients: o Hourly GCS, pupils and limb power assessment o ICP monitor (via Codman or EVD). Insert an ICP monitor if : SHI (GCS 8) with abnormal CT scan (hematomas, contusions, edema or compressed basal cisterns) SHI (GCS 8) with normal CT scan if 2 or more of the following features are noted on admission to NICU: age >40 yrs, unilat or bilat motor posturing or SBP <90 mmHg. Physiological monitors in selected patients (as ordered by neuro-intensivist): o Cardiac output monitoring: using PA catheter, PICCO (pulsed contour CO) or Cardio Q

o Continuous end tidal CO2 o Peripheral nerve stimulator (when infusions of NM blocking agents used) Neurological monitors in selected cases (ordered by NS consultant or intensivist) o Cerebral blood flow by a Laser Doppler flow probe o Brain tissue PO2 monitor (Neurotrend or Licox) o Continuous oximetric SjvO2 monoitor (refer Appendix A: SjvO2 monitoring protocol) o EEG monitoring for barbiturate coma or non convulsive seizures o Transcranial Doppler o Cerebral microdialysis (refer research protocol) o Thermodilution probe for measurement of regional CBF

SURGICAL MANAGEMENT Patients who require immediate surgical evacuation of a primary space occupying lesion (e.g. extradural hematoma) should be transferred from ED directly to the OT whenever feasible. Otherwise, they may be brought to the NICU for stabilization or to await further investigations, as may be clinically indicated.

ICU MANAGEMENT Primary aims: Avoid systemic hypotension and hypoxemia Keep CPP 60-70 mmHg and ICP <2025 mmHg Secondary aims: Keep SjvO2 >55% and PbtO2 > 20 mmHg Maintain normo-volemia and normo-tension o Order maintenance fluids: normal saline at 80-120 ml/hr (depending on size of patient). Add 10-15 ml of 7.45% KCl to each 500 ml unit if renal function normal and serum K is not raised. Avoid hypotonic fluids. o Keep MAP >80 mmHg, CVP 6-10 mmHg and urine output > 0.5-1.0 ml/kg/hr o Look for and treat causes of hypotension or hypovolemia. o Treat hypotension aggressively with fluid boluses (isotonic saline, colloids or blood).

o Start inotropes early (noradrenaline infusion: 4 mg in 100 ml D5% at 1-10 ml/hr titrated to MAP and/or CPP) to maintain perfusion pressures while catching up with volume replacement. Secure and protect the airway and decompress stomach o All intubations must be performed by an anaesthetic trainee, registrar or consultant. During office hours, page the consultant in NICU. After office hours, page the ICU registrar (Mon-Fri) or the OT anesthesia registrar (Sat, Sun and PH). For emergency cases, activate the airway pager for assistance. o Patients should be intubated via rapid sequence induction using a sedative (etomidate or midazolam) and a neuromuscular blocking agent (succinylcholine). o Confirm tube placement with auscultation. Use the capnometer when in doubt. o A CXR must be ordered to check the tube position after intubation. o Insert NG tube to decompress stomach, preferably orogastric. Ensure optimal ventilation and oxygenation. Avoid routine hyperventilaton. o Aim for normocapnia (PaCO2 35-40 mmHg) with SIMV or CMV o Keep PaO2 >100 mmHg and SpO2 >95% with appropriate FiO2 o Patients should NOT be hyperventilated routinely or prophylactically as this can further compromise already low cerebral blood flow, especially during the first 24 hrs following HI. o Hyperventilation may be used for brief periods during acute neurological deteriorations, to control intra-cranial hypertension, pending evacuation of mass lesions in the OT. Ensure adequate sedation and analgesia o Patient agitation and restlessness can lead to self extubation, dislodgement of invasive lines or excessive hypertension and worsen brain edema. o Start with a narcotic (IV morphine infusion: bolus 2-4 mg followed by 1-5 mg/hr or IV fentanyl: 25-50 g followed by 5-50 g/hr) o Add IV propofol 10-100 mg/hr (1-10 ml/hr) if patient still restless. Bolus 10-30 mg (13 ml)

o Avoid benzodiazepines as far as possible. o Reduce coughing and bucking on the ETT during tracheal suctioning by adding lignocaine (2-4% 1-2 ml) into the ETT before suctioning. Ensure neck is kept in a neutral position with the head elevated 20-30o Avoid hyperthermia. Keep rectal temperature <37.0oC o Order paracetamol 500-1000 mg q 6-8 hrly and active cooling with a cooling blanket o Add rectal voltaren 25 mg bd and ice compress to head and neck regions if still febrile o In resistant cases, consider chlorpromazine (beware BP lowering effects) PO 10-25 mg q 6-8 hrly or IM/IV 25 mg q 6-8 hrly Keep Hb 10g/dl and Na+ 140-145 mmol/L Order BS control protocol. Keep BSL 4-8 mmol/L Seizure prophylaxis o Consider anti-convulsants to prevent early (<7 days) post-traumatic seizures o Phenytoin and carbamazepine have been demonstrated to be effective. o Phenytoin: load dose is IV 15-20 mg/kg (max infusion rate is 50mg/min) followed by maintenance dose of IV 100 mg q 8 hrs (5-7 mk/kg/day). Convert to oral ON dose later. o Check phenytoin levels on D2. o Stop seizure prophylaxis after 1 week Nutrition o Start enteral nutrition EARLY (within 24-48 hrs). Start patients on gastrokinetic agents (domperidone or metoclopromide) and lactulose once enteral feeding is started. o Feed to 140% of basal energy needs in non paralysed patients and 100% of basal needs in paralysed patients, with 15% of calories as protein, by Day 7 Anti-gastritis prophylaxis o ALL patients should receive IV ranitidine 50 mg q 8 hrly or omeprazole 20 mg OM

o Once enteral feeding is established, the gastritis prophylaxis may be stopped DVT prophylaxis o All patients should receive TED stockings sequential calf compression devices o LMWH or other anticoagulants should only be used in consultation with the NS-incharge If ICP remains >25 mmHg despite the above, consider first-tier options: o Repeating CT scan to exclude new or expanding mass lesions o Order Mannitol therapy Start at 0.25-1.0 g/kg bolus followed by 100 ml 20% mannitol q 4-12 hrly Boluses are preferred to continuous infusions Check serum osmolarity daily and keep <320 mosmol/L Hypovolemia should be avoided by appropriate fluid replacements. o Drain CSF if EVD in situ o Hypertonic saline therapy Target Na+ at 145-150 mmol/L Give boluses of 100-300 ml of 3% saline, infused over 1-2 hrs via the CVP If ICP still >25 mmHg despite the first-tier options, consider second-tier options: o Decompressive craniectomy (in consultation with neurosurgeon) o Barbiturate coma (refer Appendix B: Barbiturate coma protocol) o Hypothermia therapy Active cooling to 33-34oC with cooling blanket for 24-72 hrs. (refer Hypothermia blanket protocol) Will usually need concurrent neuromuscular blockade to prevent shivering. When coming off hypothermia, advisable to rewarm to 37oC before turning off relaxants to avoid shivering. o Optimized hyperventilation (PaCO2 25-30 mmHg).

Should only be carried out with SjvO2 and/or PbtO2 monitoring to avoid cerebral ischemia caused by the hyperventilation.

INVESTIGATIONS Baseline investigations for ALL new admissions (may be omitted, at discretion of NICU MO-on-call if already done in ED or GW prior to transfer) o FBC, PT/PTT o ABG o Hypocount monitoring (frequency determined by BSL according to protocol) o U/E/Cr/Glucose (include chloride and bicarbonate) o Ca/Mg/PO4 o CXR, ECG o Liver function test (baseline) o GXM 2 units of packed cells for standby Routine daily morning labs for first 3 days o FBC, PT/PTT, ABG o U/E/Cr/Glucose, Ca/Mg/PO4 Routine daily labs after the first 3 days o ABG (daily, if intubated) o U/E/Cr/Glucose (daily if on mannitol or abnormal; if normal, may repeat 3 times per week. For patients on barbiturate coma, need to check K+ 6-12 hrly) o FBC (3 times per week) o PT/PTT (when indicated, no need for routine repeating) o Ca/Mg/PO4 (twice a week unless abnormal) o Serum osmolarity (once daily if on mannitol >twice a day) o LFT (weekly) o CXR (weekly if intubated or when clinically indicated)

SEVERE HEAD INJURY MANAGEMENT PROTOCOL CHECKLIST

Inclusion Criteria:

o SHI with post-resuscitation GCS 8 o Mod HI with GCS >8, admitted for close monitoring due to high risk for deterioration. o Post-craniotomy with brain swelling or potential for further brain swelling.
Exclusion Criteria:

o SHI with poor hemodynamics despite maximal resuscitation and unlikely to survive. o Patients with clinical and compatible CT evidence of brainstem death. o Patients with a terminal illness for which active management of the SHI is deemed futile.
INITIAL ASSESSMENT AND MANAGEMENT

o Check and stabilize ABCs. Keep MAP 80 mmHg and SpO2 >95% o Intubate ALL patients with GCS 8, if not already intubated in the ED or GW. o If patient with isolated closed HI is hypotensive, look for OTHER CAUSES of hypotension o Put cervical collar in all SHI patients until CS cleared by NS after reviewing CS x-rays o Insert ryles tube to decompress stomach
MONITORING

o Hemodynamic monitors for ALL patients: Continuous ECG, pulse oximetry, rectal temp, hourly UOP NIBP (cycle q 30 min; if no IA line inserted, cycle q10-15 min) IA and CVP lines o Neurological monitoring for ALL patients: Hrly GCS, eye signs, limb power and ICP monitor
SURGICAL MANAGEMENT: evacuate mass lesions ASAP NEUROLOGICAL MANAGEMENT

o Primary aims: Keep CPP 60-70 mmHg and ICP <20-25 mmHg Secondary aims: Keep SjvO2 >55% and PbtO2 > 20 mmHg o Maintain normo-volemia and normo-tension with CVP 6-10 mmHg and UOP 0.5-1.0 ml/kg/hr o If hypotensive, replace aggressively with normal saline, colloids and blood. o May need to start inotropes (norad) to maintain MAP while catching up with blood loss. o Aim for normocapnia (PaCO2 35-40 mmHg) and PaO2 >100 mmHg and SpO2 >95% o Ensure adequate sedation and analgesia o Keep neck neutral and head elevated at 20-30o o Keep Hb 10g/dl and Na+ 140-145 mmol/L o Order NS at 80-120 ml/hr. Add 10-15 ml of 7.45% KCl to each 500 ml unit o Avoid hyperthermia o Order anti-gastritis prophylaxis: IV ranitidine or omeprazole o Order BS control protocol (Keep BSL 4-8 mmol/L) o Order seizure prophylaxis o Nutrition: Start enteral nutrition EARLY (within 24-48 hrs) o DVT prophylaxis: TED stockings sequential calf compression device
If ICP >25 mmHg despite the above, consider the first-tier options:

o Consider repeating CT o Order mannitol therapy (0.5-1 g/kg bolus followed by 100 ml q 4-8 hrly) o Drain CSF if EVD in situ o Hypertonic saline therapy (target Na+ at 145-150 mmol/L).
If ICP >25 mmHg despite the first-tier options, consider second-tier options:

o Decompressive craniectomy (in consultation with NS) o Barbiturate coma (refer Appendix B: Barbiturate coma protocol) o Hypothermia therapy (active cooling to 33-34oC with cooling blanket + NM blockade)

o Optimized hyperventilation (PaCO2 25-30 mmHg). With SjvO2

Standard hemodynamic monitoring for ALL SHI patients: and/or PbtO2 monitoring. Continuous ECG, pulse oximetry, core temperature (rectal). Hourly urine output and I/O fluid balance All patients with or at risk of intracranial hypertension must have invasive arterial monitoring, CVP line and ICP monitor at admission to NICU. Check whether the patient is in or may be a candidate for research protocols Interventions in stage II to be targeted to clinical picture and multimodality monitoring Guidelines may be modified at the discretion of the consultant in charge Treatment grades III and IV only after approval by NICU consultant

10-15 head up, no venous obstruction CPP 60 (CVP 6-10;PAC) SpO295%; PaO2100mmHg, PaCO235-40mmHg Temp37 Blood sugar 4-7 mmol/L C; Propofol 2-5/mg/kg/hr (midazolam 0.1mg/kg/hr Morphine 0-3mg/hr or fentanyl 0.5-2mcg/kg/hr; atracurium Yes

Yes


II

ICP<20 CPP>60

No

-Recent CT - low risk of surgical lesion

Start at 0.25-1.0 g/kg bolus followed by 100 ml 20% mannitol q 4-12 hrly CardioQ/PAC, volume, vasoactivates to increase MAP (CPP 90-100) Reduce PaCO2 to 35-40mmHg CPP<60; ICP> 25 (Check probe, ? re-CT) No CT No

III

Trial bolus IV anaesthetic ( CSF if EVD propofol 50-200mg) Temp 33-34 , Drain egvasoactive agentsin situ Maintain CPP with fluids and If favourable effect on ICP and CPP start Barbiturate coma (refer Appendix B: Barbiturate coma protocol) Active cooling to 33-34oC with cooling blanket for 24-72 CPP<60; ICP> 25 hrs. (refer Hypothermia blanket protocol) (Check probe, ? re-CT)

IV concurrent neuromuscular blockade to prevent shivering V

Surgical lesion? CSF drainage? Role for surgical decompression?

Optimized hyperventilation (PaCO2 25-30 mmHg). Should only be carried out with SjvO2 and/or PbtO2 monitoring to avoid cerebral ischemia caused by the hyperventilation

Surgery Yes

Barbiturate Coma Protocol Indications: High dose barbiturate infusion(thiopentone) for: 1. Haemodynamically stable and 2. Salvageable severe head injury(GCS<8) with 3. intracranial hypertension(ICP >20-25 mm Hg) 4. refractory to maximal medical and surgical intra-cranial pressure(ICP) lowering therapies. Barbiturate coma lowers ICP by reducing cerebral metabolic demands, cerebral blood flow and cerebral blood volume. 2nd tier option in reducing ICP if ICP remains >20-25 mm Hg despite adding 1 st tier options which include: 1. 2. 3. 4. Repeating CT scan to exclude new or expanding mass lesions Osmotherapy with IV mannitol or hypertonic saline External ventricular drain insertion Mild hyperventilation

Patients who are more likely to respond: 1. Metabolic autoregulation to CO2 still intact(test by noting fall in ICP when patient is transiently hyperventilated at bedside) 2. High frequency waves still present on EEG monitoring(hence preferentially EEG monitor should be present) Prior to initiation of Barbiturate coma: 1. Order and ensure that an inotrope, preferably noradrenaline, is diluted and ready for infusion before starting thiopentone to avoid falls in MAP and CPP. 2. EEG monitoring is recommended during barbiturate coma. Initiation of Barbiturate coma: a. Dilute the thiopentone to 25mg/ml by adding 20 ml of sterile water for injection to each 500 mg bottle of thiopentone (thiopenthal) b. Loading dose Give an initial bolus of 250 mg over 10-20 min as tolerated by the patients BP. This may be repeated up to a total load dose of 500-1000 mg, according to ICP response or attainment of burst suppression on the EEG tracing. c. Maintenance dose 125-500 mg/hr titrated to ICP control or maintenance of burst suppression EEG d. End points i. Primary end-point should be ICP control. Further boluses are not needed if ICP control is achieved, even if burst suppression has not been achieved. ii. Burst suppression EEG: this can be the end-point if ICP has not been controlled after the usual loading or maintenance doses. iii. Serum barbiturate levels of 50-70 mg/dl. Routine monitoring of drug levels is not required.

Complications of Barbiturate coma: 1. HYPOKALAEMIA during induction of barbiturate coma and REBOUND HYPERKALAEMIA when the barbiturate is stopped. Check serum U/E 6 hourly. Do not correct K+ above 3.5 mmol/dl during barbiturate coma. Monitor serum U/E more regularly(i.e.1-2 hourly) during withdrawal of barbiturate coma and treat hyperkalaemia accordingly.

2. 3.

4. 5. 6. 7. 8.

Hypothermia (monitor rectal core temperature and keep above 34oC) Hypotension. Maintain CPP 60-70 mmHg with inotropes as needed One out of every 4 patients on barbiturate therapy will have clinically significant hypotension requiring vasopressors and continuous systemic monitoring. Hypotensive effect of barbiturates can offset any ICP lowering effect on cerebral perfusion pressure Myocardial depression Infections due to immunosppression by barbiturates. Actively look for clinical signs of infection as leucocytosis may be masked. Septic workup if needed. Complications of prolonged coma such as pressure sores and DVT. Gastric stasis leading to high gastric residuals with tube feeding. Hepatic and renal dysfunction

1 Morphine and other sedatives should be stopped during barbiturate coma. 2 Once ICP control has been achieved for 24-36 hrs, the thiopentone infusion may be reduced gradually and stopped. Monitor for rebound in the ICP, which may require restarting the thiopentone infusion. Patients at risk of serum potassium changes during barbiturate coma and during withdrawal of barbiturate coma: 1. Hepatic and renal dysfunction patients 2. Hypothermic patients more prone to hypokalaemia due to urinary potassium loss during cooling phase(hypothermic diuresis) 3. Acute brain injury tself may be associiated with hypokalaemia due to possibly catecholamine release 4. When barbiturate is abruptly stopped. However, difficult to explain the rebound hyperkalaemia as thiopentone has a long half life. Initiation of Barbiturate coma a. b. Dilute the thiopentone to 25mg/ml by adding 20 ml of sterile water for injection to each 500 mg bottle of thiopentone (thiopenthal) Loading dose Give an initial bolus of 250 mg over 10-20 min as tolerated by the patients BP. This may be repeated up to a total load dose of 500-1000 mg, according to ICP response or attainment of burst suppression on the EEG tracing. Maintenance dose 125-500 mg/hr titrated to ICP control or maintenance of burst suppression EEG End points i. Primary end-point should be ICP control. Further boluses are not needed if ICP control is achieved, even if burst suppression has not been achieved. ii. Burst suppression EEG: this can be the end-point if ICP has not been controlled after the usual loading or maintenance doses. iii. Serum barbiturate levels of 50-70 mg/dl. Routine monitoring of drug levels is not required.

c. d.

Commonly asked questions in Head Injury Management Questions: 1. When to do skull X-ray? 2. When to order a cervical spine X-ray? 3. When to CT scan the cervical spine? 4. When to do CT head scan? 5. When to order CT head scan for epileptics or drunks? 6. When to allow home? 7. When to admit to Observation Ward? 8. When to admit to General Ward? 9. When to admit to ICA / HDU? 10. When to admit to ICU? 11. When to intubate? 12. When to give mannitol? 13. When to hyperventilate? 14. When to give phenytoin? 15. When to feed? I. Indications for skull X-rays Antero-posterior & lateral views Townes view for occipital trauma, oblique view for suspected depressed fracture Patients with GCS 15 if : - mechanism of injury suggests a severe blow - full thickness scalp laceration or boggy haematoma - loss of consciousness (any period of time) - loss of memory - vomited - inadequate history - difficulty in clinical assessment eg. alcohol intoxication, epilepsy, children - depressed fracture or foreign body suspected All patients with GCS 13 & 14 II. Indications for cervical spine X-rays3,4,5 Antero-posterior & lateral views Open mouth view if C1 & C2 cannot be seen on a-p view In multisystem trauma, lateral view as an initial screening investigation (but needs review after resuscitation & stablisation as it does not exclude a cervical spine injury)4 GCS 15 if : - neck pain or tenderness - neurological deficit not due to an intracranial or peripheral problem - mechanism of injury suggests a spinal injury GCS 14 or less

- if normal X-rays, but significant neck pain, lateral flexion & extension views done by the patient4,5 - if normal X-rays but neurological deficit that might be caused by the cervical spine, X-ray entire spinal column (a-p & lateral views of thoracic and lumbo-sacral spine) and refer to specialist for admission4,5

III. Indications for CT scan of the cervical spine2,3 C7/T1 if not seen on plain X-rays (despite optimisation of shoulder position) C1 & C2 if GCS 8 or less, or if cannot be seen on a-p or open mouth view, to be done at time of CT head scan (need to specify on CT request form) IV. Indications for CT brain scan2,3 all patients with GCS 13 or less all skull fractures signs of skull base fracture deteriorating conscious level neurological signs seizure patients with minor head injury (i.e.GCS 15-13 with witnessed loss of consciousness, definite amnesia or witnessed disorientation) with: - persistent severe headache - persistent vomiting ( 2 episodes) - neurological signs - age > 65 years - amnesia of events before impact > 30 min dangerous mechanism(pedestrian struck by motor vehicle, occupant ejected from motor vehicle, fall from height > 3 feet or 5 stairs) - patients who fail to improve to GCS 15 after 2 hours of observation patients with GCS 13 to 14 who need a general anaesthetic for another reason eg. orthopaedic injury = periorbital bruising, subconjunctival haemorrhage, epistaxis or CSF rhinorrhoea, mastoid bruising (Battles sign), bloody or CSF otorrhoea V. Indication for CT brain scan in an intoxicated or post-seizure patient2,3 GCS 13 to 14 who fail to improve after 2 hours of observation as for above indications VI. Criteria for Discharge from Emergency Department all patients with GCS 15 with no indications for observation or admission all patients with GCS 15 with no neurological symptoms Discharge with head injury advice sheet, given to responsible 2nd person (if available)

VII. Indications for Admission to Emergency Observation Ward headache non-specific dizziness scalp haematoma, laceration, contusion, abrasion loss of consciousness soft tissue facial injury vomiting alcohol or drug intoxication unreliable or inadequate history age less than 3 (unless injury is very trivial) patients with bleeding tendencies eg. anticoagulation, thrombocytopenia Observation ward management: GCS half hourly for 2 hours, then every hour thereafter review by Senior Doctor at 4 hours (extra care of patients with bleeding tendencies) nil by mouth intravenous hydration (if clinically indicated) VIII. Indications for Admission to General Ward fracture on skull X-ray high speed injury signs of skull base fracture possible skull penetration or depressed skull fracture suspected child abuse patients on Emergency Observation ward who have been assessed by the Senior Doctor as requiring admission Inform on-call Neurosurgical Medical Officer of the admission CT brain scan if indicated General ward management: FBC, U&E, PT/PTT, Group & Save GCS half hourly for 2 hours, then every hour thereafter hourly parameters nil by mouth intravenous infusion (if clinically indicated) IX. Indications for Admission to ICA depressed (GCS 12 or less) or decreasing conscious level multiple fractures serious facial injury post-traumatic seizure severe co-morbidities

CT scan findings of intracranial pathology with significant mass effect and/or signs of brain swelling (loss of grey/white differentiation, loss of perimesencephalic cisterns, loss of cortical sulci) Contact on-call Neurosurgeon for admission ICA management: FBC, U&E, PT/PTT, Group & Save, CXR, ECG GCS half hourly for 2 hours, then every hour thereafter hourly input/output continuous ECG, BP, pulse, O2 saturation monitoring nil by mouth X. Indications for Admission to ICU all ventilated patients all patients with cardiovascular instability all patients with respiratory instability Contact on-call Neurosurgeon for admission ICU management: FBC, U&E, PT/PTT, Group & Save, CXR, ECG GCS half hourly for 2 hours, then every hour thereafter hourly input/output continuous ECG, O2 saturation monitoring, capnography invasive BP naso-gastric tube (oro-gastric if skull base fracture suspected) nil by mouth urinary catheter; peripheral temperature; CVP measurement fluid replacement with normal saline (avoid 5% glucose) 6 hourly BM stix Aim for: PaO2 greater than 60 mm Hg1 PaCO2 at chosen range but not less than 30 mm Hg1 systolic BP greater than 90 mm Hg1 ICP (if measured) less than 20 mm Hg1 CPP more than 60 mm Hg (if ICP is measured) glucose 4 to 10 mmol/l core temperature 36 to 37 0C no seizures XI. Indications for Intubation5 severe facial fractures GCS 3 to 8

PaO2 < 60 mm Hg systolic blood pressure < 90 mm Hg signs of transtentorial herniation (see below) suspicion of neurological deterioration not due to extra-cranial explanations

XII. Indications for Mannitol1 Prior to CT brain scan: TRANSTENTORIAL HERNIATION unilateral or bilateral pupillary dilatation asymmetric pupillary reactivity motor posturing (decorticate, decerebrate or no movement) PROGRESSIVE NEUROLOGICAL DETERIORATION not due to extracranial explanations After CT brain scan: intracranial pathology with significant mass effect signs of brain swelling (loss of grey/white differentiation, loss of perimesencephalic cisterns, loss of cortical sulci) Do not routinely give for extradural haematomas (as they can make them bigger) unless herniation or decreasing conscious level requiring intubation, and hence as a prelude to surgery. Administration of mannitol: urinary catheter 0.5 g per kg per dose; 20% mannitol = 20g per100mls = 5mls/g hence 70 kg = 35 g = 175 mls; give over 30 minutes; takes 15 to 30 minutes to work effect is maximal at 90 minutes and lasts for up to 4 hours; hence repeat up to every 4hrs Mannitol can produce a hyperosmolar state leading to kidney failure due to renal hypoperfusion, hence: balance input with output using normal saline (avoid hypovolaemia) daily urea & electrolytes serum osmolarity is kept below 320 mOsm (measure routinely after 2 days, and sooner if renal impairment suspected) Contraindications for mannitol: congestive cardiac failure, pulmonary oedema XIII. Indications for Hyperventilation (PaC02 30 to 35 mm Hg)1 After intubation, ventilate with tidal volume of 8 mls per kg, 10 breaths per minute, 100% oxygen and measure blood gases after 15 minutes. Keep PaCO2 at 35 to 40 mm Hg, unless:

Prior to CT brain scan: TRANSTENTORIAL HERNIATION unilateral or bilateral pupillary dilatation asymmetric pupillary reactivity motor posturing (decorticate, decerebrate or no movement) PROGRESSIVE NEUROLOGICAL DETERIORATION not due to extracranial explanations After CT brain scan: acute neurological deterioration (when surgical decompression or a repeat CT brain scan should be considered) ICP still more than 20 mm Hg (if measured), despite mannitol XIV. Indications for Phenytoin1 To prevent early (within 1st week) post-traumatic seizures in those at increased risk: seizure within 24 hours of injury GCS < 10 penetrating head wound depressed skull fracture extradural haematoma acute subdural haematoma cerebral contusion Adult loading dose = 15 mg/kg (70 kg = 1050 mg). Physician to administer 1000 mg (1g) IV at a rate of not more than 50 mg per minute with ECG & blood pressure monitoring. Side effects include cardiovascular and CNS depression, including arrhythmias, hypotension, cardiovascular collapse, respiratory arrest. Adult maintenance dose thereafter = 4 mg/kg/day (70 kg = 280 mg). Serum levels after 2 days. If dose is 300 mg or more per day, increase at 30 mg intervals (if necessary). XV. Nutrition1 replace 140% of resting metabolism in non-paralysed patients replace 100% in paralysed patients enteral better than parenteral begin no later than one week after injury 15% calories as protein resting metabolic expenditure in 25 year old male weighing 70 kg = 1700 kcal/24 hours resting metabolic expenditure in 50 year old female weighing 50 kg = 1200 kcal/24 hours monitor daily with body weight monitor twice weekly with serum albumin

Guidelines for the management of head injuries sustained after a fall by in-patients in SGH. 1. The ward HO/MO should be informed to assess the patient. 2. The assessment should include the Glasgow Coma Score (GCS), pupil size, motor power in the limbs, the presence of scalp and other injuries. The patient should also be assessed for the presence of cervical spine injury. 3. If there is clinical evidence of spinal cord injury (tetra/paraparesis or central cord syndrome) the patient should be mobilised using full spinal precautions. The neurosurgeon/orthopaedic surgeon on call should be informed to evaluate the patient. 4. If the patient has a mild head injury (GCS 14 to 15 with no neurologic deficit) he should be placed on a head chart for monitoring for 24 hours. All narcotic medications and sedatives should be withheld during this period of observation. The patient should also be kept nil by mouth during this period. The observation can be stopped after 24 hours if he is stable throughout. 5. During head chart observations any 2 point deterioration in GCS (from the best initial score), severe increase in headache/nausea or vomiting, the development of pupillary inequality, motor deficits or seizures must be evaluated by CT brain scan and neurosurgical consultation. 6. A patient who develops signs such as a racoons eye, Battles sign, CSF rhinorrhea/otorrhea or a delayed cranial nerve palsy must also be evaluated by the neurosurgeon. 7. All patients with GCS <= 13 and/or with neurologic signs after head trauma must be evaluated with a CT brain scan and reviewed by the neurosurgeon. 8. Simple scalp injuries can be treated with toilet and suture on the ward. Antibiotics should be reserved for contaminated injuries or injuries left exposed for > 3 hours. More complex injuries must be evaluated by the neurosurgeon/plastic surgeon.

Subarachnoid Haemorrhage (SAH) Risk factors Smoking appears to be a significant risk factor, as does heavy alcohol consumption. Data regarding the relationship between hypertension and SAH are conflicting. Clinical grading scales Clinical assessment of SAH severity commonly utilizes grading scales. The 2 clinical scales most often employed are the Hunt and Hess and the World Federation of Neurological Surgeons (WFNS) grading systems. A third, the Fischer scale, classifies SAH based on CT scan appearance and quantification of subarachnoid blood. Hunt and Hess grading system Grade 1 - Asymptomatic or mild headache Grade 2 - Moderate-to-severe headache, nuchal rigidity, and no neurological deficit other than possible cranial nerve palsy Grade 3 - Mild alteration in mental status (confusion, lethargy), mild focal neurological deficit Grade 4 - Stupor and/or hemiparesis Grade 5 - Comatose and/or decerebrate rigidity

WFNS scale, World Federation of Neurological Surgeons Grade 1 - Glasgow Coma Score (GCS) of 15, motor deficit absent Grade 2 - GCS of 13-14, motor deficit absent Grade 3 - GCS of 13-14, motor deficit present Grade 4 - GCS of 7-12, motor deficit absent or present Grade 5 - GCS of 3-6, motor deficit absent or present Fisher scale (CT scan appearance) Group 1 - No blood detected Group 2 - Diffuse deposition of subarachnoid blood, no clots, and no layers of blood greater than 1 mm Group 3 - Localized clots and/or vertical layers of blood 1 mm or greater in thickness Group 4 - Diffuse or no subarachnoid blood, but intracerebral or intraventricular clots are present The Hunt and Hess and the WFNS grading systems have been shown to correlate well with patient outcome. The Fisher classification has been used successfully to predict the likelihood of symptomatic cerebral vasospasm, one of the most feared complications of SAH. All 3 grading systems are useful in determining the indications for and timing of surgical management. For an accurate assessment of SAH severity, these grading systems must be used in concert with the patient's overall general medical condition and the location and size of the ruptured aneurysm.

Indication for intervention (endovascular coiling and surgical clipping) The indications for surgery in patients with SAH can be stratified based on clinical grade. Other factors, such as overall medical condition of the patient, aneurysm size, location and accessibility of the aneurysm for surgical repair. For patients with a mild- or intermediate-grade SAH (Hunt and Hess/WFNS grades 1-3), aneurysm treatment is strongly recommended because the risks of SAH complications greatly exceed the risk of endovascular/surgical intervention. If the endovascular anatomy and clinical situation is suitable, aneurysm coiling will be offered. If endovascular treatment is not suitable then surgery will be offered. For patients with a poor grade of SAH (Hunt and Hess/WFNS grades 4-5), the decision whether to operate is controversial and decided by the surgeon in charge. The overall outcome is poor, with or without surgical intervention. However some studies have reported up to 15% good outcome. Other indications for surgical management include the following: Wide-necked aneurysms (unsuitable for endovascular intervention) Mass effect or hematoma associated with the aneurysm (surgery needed to evacuate the clot) Recurrent aneurysm after coil embolization Management Protocol of Aneurysmal Subarachnoid Haemorrhage in NNI-SGH NICU PRE-OPERATIVE MANAGEMENT All patients with acute spontaneous subarachnoid haemorrhage (SAH), confirmed on CT scan (non contrast) should be admitted to the NICU or Neuro HD for: Close neurological monitoring. Neurological deterioration may occur from: 1. Rebleeding (4% on 1st day, 1-2% per day x 4 weeks or 20-30% for 1st month then about 3% per year after 3 months) 2. Hydrocephalus 3. Delayed cerebral ischemia Close monitoring and control of the blood pressure and volume status Intubation and controlled ventilation for patients with GCS 8 (grade IV & V) Close monitoring for potentially life-threatening arrhythmias. 1. Airway Management and Ventilation Decision made regarding intubating patient Intubate under controlled conditions with sedation, neuromuscular paralysis and cricoid pressure to prevent pulmonary aspiration and surges in blood pressure. Target PaCO2 35-40 mmHg, PaO2 >80 mmHg and SpO2 >95% 2. Hemodynamic Management Insert arterial lines in ALL patients for close monitoring of BP Maintain euvolaemia and target systolic BP at 120-160 mmHg (or otherwise ordered by NS or ICU Consultant-in-charge) BP control; Aim to keep BP within target range without BP surges. If BP not controlled within target range after adequate analgesia and sedation, start

anti-hypertensive therapy 3. Sedation and analgesia Aim to keep patient calm and rested. Excessive agitation increases risks of aneurysmal rebleeding. Severe headache: start paracetamol 1 g q 6 hrly and/or IM codeine 30-50 mg q 4-6 hrly If patient is restless or agitated, initiate morphine therapy. Bolus with 1-2 mg q 15-20 min (max 4-8 mg) followed by infusion at 0.5-3.0 mg/hr Add IV propofol infusion at 10-100 mg/hr if patient still restless or additional sedation needed (e.g. during angiogram) 4. Neuroprotection Start Nimodipine therapy: Oral nimodipine unless contraindicated PO nimodipine 60mg q 4 hrly (start with 30mg q 2-4 hrly if SBP 120 mmHg) IV nimodipine 2 mg/hr or 10 ml/hr, together with 40 ml/hr of normal saline through central line (reduce dose if SBP 120 mmHg) Seizure prophylaxis; Start prophylactic anti-epileptics in all patients o Phenytoin: load dose of IV 15-20 mg/kg over 20-30 min (max rate of 50mg/hr) followed by 100 mg q 8 hrly o If allergic to phenytoin, start carbamazepine or sodium valproate. 5. Diagnosis and localisation of cerebral aneurysm The NS MO must accompany all intubated patients during transfer to and from the angio suite and during the angiogram procedure. GDC Coiling of cerebral aneurysms require GA during the procedure. 6. Common complications in patients with aneurysmal SAH Cerebral salt wasting o Present with hypovolemia, hyponatremia and high urine Na+ o Correct with hypertonic saline (100-300 ml 3% saline, then check Na+ level) Cardiac arrhythmias o Ventricular and atrial ectopics are commonly encountered. o Treat if a/w hemodynamic effects Myocardial ischemia;Do 12 lead ECG, cardiac enzymes o If cardiac function affected, may refer cardiology for risk assessment and/or 2-D echo examination. 7. o o General ICU Care Fluid therapy Anti-gastritis prophylaxis Once enteral feeding is established, the gastritis prophlaxis may be stopped DVT prophylaxis All patients should receive TED stockings

OPERATIVE MANAGEMENT Good grade and medically fit patients should receive early treatment of the aneurysm. 1. Suitable cases may be referred for coiling (decided by vascular neurosurgeon-incharge) 2. Poor grade or medically unfit patients may be managed conservatively. 3. If hydrocephalus present, insert EVD 4. Poor grade patients with hydrocephalus may improve following EVD insertion. These should be re-evaluated for surgical management. POST-OPERATIVE MANAGEMENT All patients with completely clipped aneurysm/s and no other unsecured aneurysms should receive prophylactic TRIPLE H THERAPY after surgery HYPERTENSION - Target SBP >160 mmHg or CPP >60 mmHg (if ICP monitored) - Lower or higher BP targets may be chosen as decided by NS or ICU consultant. - IV noradrenaline infusion may be started if BP goal still not achieved after multiple fluid boluses (NA 4 mg in 100 ml NS at 1-10 ml/hr) HYPERVOLEMIA Keep CVP 8-12 mmHg if achievable HEMODILUTION Do not transfuse patients above Hb 10 g/dl or hematocrit >30-35% 1. IV nimodipine 2mg/hr for 1-2 weeks via CVP followed by PO 60 mg q 4 hrly - Total therapy of 3 weeks (The neurosurgeon in charge may opt to oralise the medications earlier if the clinical situation permits) 2. Nutrition Start enteral nutrition EARLY (within 24-48 hrs) once all planned surgical procedures have been completed. 3. Post operative TCD 4. Delayed cerebral ischaemia: - Manifests as gradual decrease in GCS and / or new hemiparesis - Repeat CT scan to rule out rebleed, IC haematoma, cerebral oedema, hydrocephalus - The management is now therapeutic Triple H therapy. 5. Hydrocephalus - Treated by EVD or Lumbar Drain as decided by Neurosurgeon The goal of Triple H Therapy is to raise cerebral perfusion pressure to reverse the neurologic deficit. However the therapy may be limited if : i) There is poor myocardial tolerance ii) The therapy precipitated brain swelling or a rise in ICP iii) There are remaining aneurysms which have not been secured.

The therapy may be delivered in ICA/ICU. A cardio-Q cardiac output monitor may be helpful in assessing treatment. Cerebral aneurysms Prevalence of 5%. About 50% of aneurysms rupture. Only 2% present during childhood. Eitology 1. Congential predisposition 2. Atherosclerotic or hypertensive 3. Embolic 4. Infectious (mycotic) 5. traumatic 6. Others Location 85-95% in carotid system( anterior circulation) i. ACoA single most common 30% ii. P-comm 25% iii. MCA 20% 5-15% in Vetebrobasilar circulation( posterior circulation) i. Basilar artery, basilar bifurcation -10%Followed by BA-SCA, BA-VA junction, AICA 20-30% - multiple aneurysms Clinical presentation Intraventricular haemorrhage(IVH) occurs in 13-28%; bad prognosis with IVH o A-comm- IVH by rupture through lamina terminalis into ant. #rd or lat. ventricles o Distal basilar or carotid terminalis- IVH by rupture through floor of 3rd ventricle o Distal PICA- rupture directly into 4th ventricle via foramen of Luschka. Mass effect causing signs and symptoms o Brainstem compression hemiparesis o Cranial nerves palsies o Endocrine dysfunction form intra/suprasellar aneurysms Headaches- from minor haemorrhage sentinel bleed o Acute thunderclap, worst headache of my life ; o Subacute - from raised ICP or dura irritation TIA from distal embolisation Seizures Incidental finding from angiography or neuroimaging Associated conditions/ syndromes Autosomal Dominant Polycystic Kidney Disease Fibromuscular dysplasia AVM , Moyamoya disease Familial cranial aneurysm syndrome Co-arctation of aorta Osler-Weber-Rendu syndrome Atherosclerosis; bacterial endocarditis

SAH Protocol Checklist


PRE-OPERATIVE MANAGEMENT
Airway and ventilation

o Intubate if GCS 8. o Target PaCO2 35-40 mmHg, PaO2 >80 mmHg and SpO2 >95%
Hemodynamic Management

o Insert IA line o Target systolic BP at 120-160 mmHg. Control BP with IV labetolol if high
Sedation and analgesia

o Keep patient calm and rested. o Start IV morphine (0.5-3.0 mg/hr) IV propofol (10-100 mg/hr or 1-10 ml/hr)
Start Nimodipine:

o No CVP: PO nimodipine 60 mg q 4 hrly (30 mg q 2-4 hrly if SBP 120 mmHg) o With CVP: IV nimodipine 2 mg/hr together with 40 ml/hr NS via CVP
Fluids: order IV NS 80-120 ml/hr + KCl to maintain euvolemia Order seizure prophylaxis: load phenytoin (IV 15-20 mg/kg over 20-30 min) foll by 100

mg q 8 hrly
Order anti-gastritis prophylaxis: IV ranitidine or omeprazole Arrange for 4 Vessel Angiogram Look out for cerebral salt wasting, cardiac arrhythmias and evidence of myocardial

ischemia
Ensure DVT prophylaxis: TED stockings sequential calf compression devices for all

patients

POST-OPERATIVE MANAGEMENT
Transfer post-op orders Check with surgeon that aneurysm has been completely clipped Order prophylactic HYPERVOLEMIA for ALL patients if there are no residual unclipped

aneurysms and no medical contraindications present: o IV NS 100-140 ml/hr (2.5-3.0 L/day) and keep CVP 8-12 mmHg, if achievable o Colloid boluses with gelafundin 200 ml or albumin 5% 250 ml prn or q 6-8 hrly
Order DAILY TCDs for all patients Continue nimodipine therapy: IV 2mg/hr for 1-2 weeks via CVP followed by PO 60 mg q 4

hrly for a total of 3 weeks


Nutrition: start enteral nutrition EARLY. When there is TCD evidence of vasospasm or if ordered by NS consultant, start

HYPERTENSIVE therapy also o Target SBP >160 mmHg and start IV NA 4 mg in 100 ml NS at 1-10 ml/hr if necessary. o BP targets may be raised or lowered by the NS or ICU consultant.
Do not transfuse patients above Hb 10 g/dl or hematocrit >30-35% Delayed cerebral ischemia (VASOSPASM): usually p/w GCS and/or new hemiparesis.

o Repeat CT scan to rule out re-bleed, ICH, cerebral edema or hydrocephalus o If MCA velocity >150 cm/s, MCA/ICA velocity >3 and patient asymptomatic: Maintain triple H at present targets and monitor neurological status closely o If MCA velocity >150 cm/s, MCA/ICA velocity >3 and patient develops new neurological deficits or GCS falls:

Raise BP target to SBP >200 mmHg start or step up IV noradrenaline Step up IV fluids (NS infusion rate boluses of gelafundin or albumin 5%) If neurological deficits do not improve after 60 min, inform NS and consider urgent angiogram. Neuroradiologist may perform angioplasty or inject papaverine.

Artriovenous malformations
The incidence and prevalence of intracranial vascular malformations are not known with certainty. Autopsy data suggest that there is an overall frequency of detection of AVMs in 4.3% of the population. In another autopsy series, 46 AVMs were noted among 3200 brain tumor cases, for a frequency of detection of 1.4%; 12.2% of the cases were symptomatic

Grading Systems and Risk of Therapy


Grading schemes were initially developed as a means to predict surgical risk during obliteration. The important variables include size, number of feeding arteries, velocity of flow through the lesion, degree of steal from surrounding brain, location (including surgical accessibility), eloquence of adjacent brain, presence of associated aneurysms, and finally, the pattern of venous drainage. The Spetzler-Martin grading scale has also been applied prospectively. Lesions graded I, II, or III were found to have low treatment-associated morbidity. Surgery should be strongly considered as the primary mode of therapy for Spetzler-Martin grade I and II lesions. For patients with small lesions, where surgery offers some increased risk based on location or feeding vessel anatomy, radiosurgery should be strongly considered. Surgical management for Grade III lesions should be treated on a case-by-case basis. Grade IV lesions conferred 31.2% treatment-associated morbidity, and grade V lesions had 50% new treatmentassociated morbidity. In addition, the rate of permanent deficit was 29.9% for grade IV lesions and 16.7% for grade V lesions. Surgical treatment only is often not recommended for grade IV and V lesions because it confers a high risk.

Grade IV and V lesions require a multidisciplinary approach with individual analysis


Spetzler-Martin AVM Grading Scale
Size 03 cm 3.16.0 cm .6 cm 1 2 3 Location Noneloquent Eloquent Deep venous drainage Not present Present 0 1 0 1

Treatment Options
At present, there are 4 major treatment options available for patients with an AVM of the brain. 1. single therapy 2. combined therapy applying microsurgery

3. 4.

endovascular techniques radiosurgery (focused radiation).

The lesion can be monitored expectantly with the understanding that the patient would have some risk of hemorrhage or other neurological symptoms such as seizures or focal deficit. Alternatively, intervention can be undertaken with the goal of complete AVM obliteration, because subtotal therapy does not confer protection from hemorrhage. AVM surgery is usually elective and frequently preceded by preoperative embolization. The surgical approach allows complete resection of the nidus, resecting the feeding vessels and subsequently the draining veins. Management of associated aneurysms is determined on an individual basis.

Postoperative Care
The recommendations for postoperative care include: 1. Neurological intensive care monitoring for at least 24 hours. 2. Blood pressure is monitored with an arterial catheter 3. Urine output is monitored with an indwelling catheter. 4. Typically, normotensive and euvolemic conditions are maintained 5. Tight blood pressure control with agents that do not act in the central nervous system may be appropriate for selected individuals. 6. Perioperative antibiotics, steroids, and seizure medication. 7. An angiogram is also performed to confirm complete resection of the AVM during the immediate postoperative period. 8. A new neurological deficit after surgery is usually investigated with a CT scan to rule out a hemorrhage or hydrocephalus. 9. MRI scanning with diffusion-weighted imaging may be appropriate if an infarction is entertained.

Endovascular Treatment
Indications for embolization can be divided into presurgical embolization in large or giant cortical AVMs and embolization before radiosurgical intervention to reduce nidus size. In addition, palliative embolization may be used in large nonsurgical or nonradiosurgical AVMs in patients presenting with progressive neurological deficit secondary to high flow or venous hypertension. Flow-directed and flow-assisted microcatheters have made navigation of intracranial vessels safer and have allowed more accurate delivery of embolic materials. Current embolic materials are divided into solid or liquid agents. Solid agents consist of polyvinyl alcohol particles, fibers, microcoils, and microballoons. Liquid agents consist of cyanoacrylate monomers such as IBCA (I-butyl cyanoacrylate) and NBCA (N-butyl cyanoacrylate), as well as polymer solutions such as ethylene vinyl alcohol (EVAL copolymer).

Management of Complications
Hydrocephalus Insertion of ventricular drainage catheters may be necessary. These catheters can also be used to monitor intracranial pressure in patients in the intensive care unit setting. Patients may have chronic hydrocephalus and thus may warrant ventriculoperitoneal shunting. Seizures Obliteration of AVMs may reduce the incidence of seizures. No studies exist from which recommendations can be made in terms of duration or type of anticonvulsant prophylaxis after treatment.

Spontaneous ;Non-traumatic Intracerebral Haemorrhage(ICH) Triage: Good GCS (15-13) Moderate GCS (12-9) Poor GCS (8-3) Good GCS patients 1. History - onset, progression - hypertension, DM, lipid, IHD, previous CVA, malignancy, smoking
- drugs esp antiplatelets, anticoagulants.

2. Exam - Basic and complete neurologic exam. Basic general exam. 3. CT scan - site of haematoma putamen, thalamus, caudate, parenchymal, superficial lobar(state which lobe), midbrain, pons, cerebellum. - size of haematoma - 1/2 (length x breadth on largest CT slice) x height - any ventricular extension, any hydrocephalus. 4. Investigation - FBC, U/E, PT/PTT, GXM, CXR, ECG. Management Acutely - Mx in GW unless BP control poor needing IV labetolol ICA - Hrly CLC, NMB for 24 hrs - control BP to keep systolic < 160-180 mmHg - correct any coagulopathy rapidly. Consult hematology if necessary. Later - bring BP to target range over a few days. (In general the target is </= 140mmHg systolic initially if patient hypertensive), if patient is normotensive, aim for systolic

BP </= 120mmHg. Watch for giddiness and postural hypotension). - Identify other risk factors for cerebrovascular disease including fasting lipids, fasting sugar, post prandial sugar as appropriate. - Arrange further invx MRI, angiogram as directed by neurosurgeon i/c. - Physiotherapy, speech therapy, MSW, Rehab review as appropriate. Referral to smoking cessation clinic for smokers. - DVT prophylaxis TED stockings infections investigation and treat as appropriate BP control in ICH patients Use S/L Nifedipine 5- 10 mg initially. If there is no response or if BP remains above 160180mmHg then consult neurosurgeon in charge re: starting labetolol.
IV Labetolol.

To be used in ICA or ICU only. Onset of effect in 1 minute, peak effect in 20 minutes. Does not cause cerebral vasodilation or rise in ICP Contraindications as per other beta-blockers. Nurses will prepare 1mg/ml solution Boluses of 5 10 mg every 15 to 20 minutes until BP control achieved. Then run infusion starting @ 5mg per hour to maintain control. Moderate GCS patients Same as for good GCS patients. In addition: Assess if GCS score is due to raised ICP. Aphasic patients will score GCS10 at best. Signs: Unequal pupils Severe headache, vomiting multiple episodes BP > 200mmHg systolic Bradycardia <70 bpm CT: clot volume >30 ml. Cerebellar clot > 3cm in maximum diameter Hydrocephalus due to intraventricular bleeding Midline shift, uncal herniation seen Obliteration of perimesencephalic spaces. Management - ICA kiv ICU. Neurosurgeon in charge may decide on general ward management. - consult neurosurgeon on use of mannitol, prophylactic phenytoin(for lobar ICH only) - if GCS drops further by 2 pts or more, or if neurologic deficit worsens or new neurologic develops transfer to ICU kiv intubation as ordered by neurosurgeon consult neurosurgeon on call re: - need for repeat CT scan

- use of IV mannitol, phenytoin. - need for operation, arterial line, CVP line. Poor GCS patients - Decision to intubate/not intubate by neurosurgeon based on age, premorbid status, concurrent chronic illness, involvement of dominant hemisphere, extensive brain damage seen on CT (e.g. clot extending into midbrain) etc. - Decision for operation/no operation by neurosurgeon. - Mx in GW/ICA/ICU as decided by neurosurgeon. Discharge planning Home (may be with maid application/training), AMK slow stream Rehab, SGH inpatient rehab, Nursing home.

Intracranial Haemorrhage secondary to anticoagulants Various studies have suggested that anticoagulation increases the risk of intracranial haemorrhage by 7-10 fold, to an absolute risk of 0.3-1% per year. The mortality associated with oral anticoagulant related intracranial haemorrhage is about 60%. There is often confusion over whether the risk of valve thromboembolism from reversing anticoagulation outweighs the benefit of arresting any continuing bleeding. It has been suggested that intracranial haemorrhage occurring while on warfarin may continue to evolve over 24 hours in 50% of patients. This is by contrast with non-anticoagulated patients in whom only 10% of haemorrhages continue to enlarge in the first 24 hours. Thus if treatment is given to reverse the coagulopathy it should be given as rapidly as possible. Anticoagulation with warfarin can be reversed with vitamin K, fresh frozen plasma, or factor concentrates. Warfarin reduces the availability of vitamin K and thereby reduces the concentration of the vitamin K dependent clotting factors (II, VII, IX, and X). Vitamin K is always required to achieve more than a temporary reversal of anticoagulation, but takes 4-6 hours to work. A dose of 5-10 mg is recommended for life threatening haemorrhages such as intracranial bleeding. There is often reluctance to use vitamin K because it can result in warfarin resistance and difficulty in reanticoagulating the patient. Vitamin K does not affect subsequent use of heparin. As synthesis of clotting factors after vitamin K takes several hours, coagulation factors should also be replaced directly. Fresh frozen plasma is the standard treatment used (15ml Kg); the alternatives are individual factor concentrates. Current guidelines on the reversal of warfarin anticoagulation in the event of intracranial haemorrhage are not based on prospective randomised trials: none have been done. Having reversed anticoagulation, it is uncertain when to recommence it. There are no prospective studies. However, if the risk of embolism from prosthetic heart valves resulting in major stroke or death is 4% a year and the risk of valve thrombosis is 1.8% a year, the daily risk can be estimated to be 0.016%. Thus stopping anticoagulation for 6 weeks is associated with a risk of major stroke or death of 0.67%. The decision to reintroduce anticoagulation should be based on the balance between a patient's thromboembolic risk and their bleeding risk. Management Guidelines 1) Admit to NICU/ICA. 2) Avoid setting central lines if INR prolonged more than 1.5. IA lines may be set. 3) Phenytoin loading (if appropriate) 4) Mannitol if needed; IV Vitamin K 5-10mg. 5) IV FFP (15ml/kg) given rapidly with IV lasix if needed. Time is of essence. Ideally infusion should be started from A&E. Watch for signs of fluid overload. 6) Continue correction till INR less than 1.5. 7) Proceed to Surgery if indicated 8) If platelet transfusion is required, the platelets are to be infused in the ward/ICU/ICA immediately after collection from the blood bank. Then inform the OT to call for the patient ASAP (therapeutic window = 24 hrs). Confirm the amount of platelets required with hematologist/neurosurgeon.

Endocrinology Syndrome of Inappropriate Antidiurecric hormone secretion (SIADH) Release of ADH in absence of physiological stimuli Resulting in hyponatremia with high urine osmolarity Usually accompanied by hypervolemia, sometimes euvolemia Important to distinguish from cerebral salt wasting Associated with certain malignancies and many intracranial abnormalities Causes of SIADH 1. Malignant tumors esp. bronchogenic tumors 2. Intracranial pathology meningitis, trauma, tumors raised ICP, SAH 3. Infections e.g. TB, aspergillosis 4. Drugs oxytocin, thiazides, carbamazepine, chlorpropamide 5. Others stress, anaemia, nausea, any cause of hypotension, acute int. porphyria Diagnosis Criteria 1. Low Na+ : <134mmol/L 2. Low serum osmolality : <280mOsm/L 3. High Urine Na+ : >18m Eq/L 4. High Urine: serum osmolality: often 1.5-2.5:1 5. Normal renal ; adrenal; thyroid function 6. No signs of dehydration over overhydration Test : water load test. (Not for pts with serum Na+<124mmol/L). Give pt 20mls/kg(max 1.5L) water load orally, in the absence of adrenal/renal dysfunction, the failure to excrete 65% of load in 4hrs or 80% in 5hrs indicates SIADH. Symptoms of SIADH Symptoms of hyponatremia- confusion. Lethargy, N+V, coma Paradoxical thirst; possibly fluid overload Treatment of acute SIADH 1. look for underlying cause and treat it .e.g. treat infections, transfuse if anaemic 2. If mild and asymptomatic : Fluid restriction <1L/day 3. If severe or symptomatic consider hypertonic saline 3%. Consult registrar or consultant prior starting. Be caution of excessive rapid correction, Central pontine myelolysis may occur. Treatment of Chronic SIADH 1. Long term fluid restriction 1.2-1.8L/day 2. Demeclocyclibne 150-300mg PO 6H 3. Furosemide(Lasix) 40mg PO OM 4. Phenytoin- may inhibit ADH release If in doubt, consult an endocrinologist for help.

Cerebral Salt wasting(CSW) Renal loss of sodium as a result of intracranial pathology, producing hyponatremia and decrease in ECF. Beware in pts with SAH, they may have CSW with hyponatremia that mimics SIADH. Fluid restriction may exacerbate vasospasm induced ischemia. CSW negative present present SIADH Variable Absent /N /N +/Hematocrit Parameters Serum osmolality Serum BUN: creatinine Serum Protein Urinary sodium Serum Potassium Serum Uric acid CSW /N N SIADH N N /N

CSW and SIADH Parameters Plasma volume Salt balance Dehydration Weight PCWP CVP Orthostatic hypotension

: Increased; : Decreased; N : Within normal limits; +/-: may or may not be present Treatment of CSW 1. Volume replacement and positive salt balance. Hydrate pt with 0.9% N/S or sometimes 3% NaCl. Salt may also be replaced orally e.g. NaCl tabs 2-3 tabs bd. 2. Rapid correction of sodium levels is associated with central pontine myelolysis, so take caution esp. with 3% NaCl. Do not correct > 10mmol/L in 24hrs. 3. Fludrocortisone acetate acts directly on renal tubules to increase Na+ absorption. 0.2mg IV or PO has shown benefits but may cause hypt, pulm. edema or hypoK+

DIABETES INSIPIDUS (DI)


Deborah Tan
CLINICAL Excretion of abnormally large volumes of dilute urine (Normal urine output = 0.5-1ml/kg/hr). o Polyuria = 200ml/hr for >3hrs or >50ml/kg/d. o 24h Urine concentration <300mOsm/L in the absence of excessive glucose or other solutes. Urinary frequency, enuresis, nocturia, polydipsia. Hypotension due to dehydration. (in patients with impaired fluid intake). Rule out primary polydipsia. (e.g. psychogenic). Exclude other causes of polyuria e.g. excessive IV fluids, mannitol infusion, hyperglycemia. CENTRAL (CRANIAL) DI = hypothalamic or pituitary lesion resulting in ADH deficiency (<80-85% normal). Causes: Head trauma Iatrogenic: pituitary surgery Space occupying lesion: craniopharyngioma, large pituitary tumour Infection: meningitis, viral encephalitis, toxoplasmosis Inflammatory: Wegeners granulomatosis, SLE, scleroderma Infiltrative: saroidosis, autoimmune hypophysitis. Ischemia: Sheehans, aneurysm Congenital Pregnancy (vasopressinase) Idiopathic IV or S/C DDAVP 0.03ug/kg increase of >50% in urine osmolality 1-2hrs later indicates central DI. Serum osmolality >295mOsm/kg. Ratio of urine to serum osmolality <2 in paired blood and urine samples. Further investigations: MRI brain Tests of anterior pituitary function (e.g. thyroid). Treatment: Treatment of choice: Desmopression (DDAVP) L-arginine vasopressin synthetic analogue. IV/SC DDAVP 1-4ug q12-24h. (stat 1-2 microgrammes iv ) Intranasal DDAVP 5-20ug q8-12h (avoid IN route 12wks post transphenoidal surgery). Nasal pump delivers 10ug/spray. PO DDAVP 0.1-0.2mg q8-12h (but absorption erratic). INVESTIGATIONS Serum and urine osmolality Serum Ur/Cr/E/Glu, Ca2+, PO43-, albumin Hourly urine output and fluid intake

NEPHROGENIC DI = renal insensitivity to ADH. Causes: Drugs: lithium, aminoglyosides, cisplatin, methoxyflurane, amphotericin B, rifampin. Renal: obstructive uropathy Electrolytes: hypokalemia, hypercalcemia Ischemic: sickle cell, acute tubular necrosis Infiltrative: amyloidosis Congenital: defects in ADH receptors/pathways mediating anti-diuresis.

Further management points: Strict I/O monitoring. Avoid water intoxication: judicious fluid administration (match urine output and insensible losses) + frequent serum sodium and osmolality monitoring. Allow oral fluids if possible so that patients fluid intake is guided by thirst. Note: possible triple phase response in first 4-6 weeks post-surgical or traumatic DI initial DI followed by SIADH with/without return of permanent DI.

Fluids and Electrolytes All that is lost must be replaced Total 60% of Body Wt Total Body water a. Intracellular 40 % 1/3 b. Extracellular 20 % 2/3 b.i Intravascular 5% 1/3 x b.ii. Interstitial 15 % 1/3 x Components of Fluids and Electrolyte Treatment 1. Maintenance volume requirements 2. On going losses 3. Volume excess or deficits 4. Maintenance Electrolyte requirements 5. Electrolytes excess of deficits 1. Maintenance volume requirements 1. 1st 10 kg 100 ls/kg/day i.e. nd 2. 2 10 kg 50 mls/kg/day 3. Subsequent Kg 20 mls/kg/day

70 kg 28 Litres 14L 3.5L 10.5L

50kg - 2100mls/day 60kg - 2300mls/day 70kg 2500mls/day

2. On going losses 1. Calculate from recordable losses e.g. NG, Drains, Fistulae, 3rd Space(Estimate) 2. Insensible losses 10 mls/kg/day 3. Replace ongoing losses with isotonic solution i.e. 0.9% Normal saline 3. Volume excess or deficits 1. Deficits a. Acute : Low urine output/ low CVP, tachycardia, Hypotensive b. Chronic : Decreased skin tugor, sunken eyes, oliguris, orthostatic hypotension, Increased HCT, Increased BUN/Creatinine ratio 2. Excess a. Overhydration, mobilisation of 3rd space losses, Pulmonary edema, peripheral edema, S3 gallop, positive I/O 3. Assess clinically and watch I/O charting, CXR for pleural effusion. 4. Maintainence Electrolyte Requirements 1. Na+ : 1- 2 mEq/Kg/Day a. Replace slowly if low < 12mmol/day with 0.9% N/S or NaCl tabs 2. K+ : 0.5-1 mEq/Kg/Day a. Replace with IV Premix 10mmol or 20 mmol in 100mls, slow infusion or Mist KCL 5-10mls tds if patient is tolerating diet well. 5. Electrolytes excess or deficits 1. Na+ deficits : 140-(Actual Na+) x 0.6 x Body weight(Kg) 2. K+ deficits : 4 (acutal K+ ) x 0.6 x Body weight(Kg)

3.

Ca2+ Levels

:[(40- albumin levels) x 0.02] + Ca2+ levels(total)

Fluids and Electrolytes


Hyperkalemia (K > 5.0mmol/L)

Transcellular shifts Acidosis Beta-blockers Insulin deficiency Succinylcholine

Increase in body stores

Increased cell count or cell lysis Haemolysis Leucocytosis (>50k) Thrombocytosis (1000k) Rhadomyolysis Tumour lysis

Excess intake K supplements Massive blood transfusion

Impaired excretion Renal failure Drugs: ACE inhibitors K sparing diuretics NSAIDS

Diagnostic approach to hyperkalemia 1. 2. 3. 4. Hyperkalemia is serum K > 5.0mmol/L. A haemolysed blood sample can result in a falsely elevated K reading. Hyperkalemia can be due to increase in total K stores or shifting of K out of cells. Non transcellular-shift causes of hyperkalemia may be caused by: a. Cell lysis b. Impaired excretion c. Excessive intake

Clinical effects 1. ECG changes: Tall T waves, prolonged PR interval, loss of P waves, widened QRS, VT, VF and cardiac arrest. 2. Neuromuscular weakness, areflexia, paralysis and parasethesia. Treatment approach 1. Hyperkalemia may result in life-threatening arrhythmias and should always be monitored and treated. 2. Direct membrane antagonism to prevent cardiac toxicity a. IV 10% CaCl 10ml should be given over 2-5min, preferably via a central line b. Alternatively, IV Ca gluconate may be given 3. Transcellular shift of K into cells a. IV insulin 5-10units with IV dextrose 50% 40ml b. IV NaHCO3 50 100mEq infused over 5-10min 4. Enhance clearance from the body a. Diruretics: IV frusemide 10-20mg b. Ion exchange resins (Resonium PO 15g q8h or PR 30g q8h) c. Haemodialysis

Hypokalemia (K < 3.5mmol/L)

Transcellular shifts Insulin administration Glucose administration Alkalosis Beta-agonist therapy

Decreased total K stores

Measure urinary K

Extrarenal losses (Urine K <30mEq/L) Vomiting Diarrhoea NG losses

Renal losses (Urine K >30mEq/L) Diuretics Mg depletion Dehydration Mineralocorticoid excess Alkalosis AmphotericinB

Diagnostic approach to hypokalemia 5. Hypokalemia is serum K < 3.5mmol/L. 6. Hypokalemia can be due to decrease in total K stores or shifting of K into cells. 7. Non transcellular-shift causes of hypokalemia can be differentiated by measuring urinary K levels: a. Extrarenal losses of K will result in renal conservation of K, hence urinary K will be low (<30mmol/L). b. Renal losses of K will result in high urinary K levels (>30mmol/L). Clinical effects 3. ECG changes: flattened or inverted T waves, U waves, atrial & ventricular arrhythmias (e.g. PACs, PVCs). 4. Neuromuscular weakness, ileus, paralysis 5. Renal: Mg depletion, nephrogenic diabetes insipidus Treatment approach 5. Replacement solutions must never be given as an IV bolus. 6. Replacement solutions: a. 7.45% KCl has 1mEq/ml of K b. KH2PO4 has 1mEq/ml of K and 1mmol/L of PO4 7. Replacement rate: 10-30mEq/hour in 100-200ml NS or D5%. Premixed KCl (20mmol of K in 100ml NS) is commonly used. 8. Replacement solutions are hyperosmolar and should preferably be given via a central line.

Hypernatremia (Na >145mmol/L)

Assess ECF volume

Hypovolaemic

Euvolaemic

Hypervolaemic

Renal losses Diuretics Osmotic diuresis Mannitol, glucose Diabetes insipidus Extrarenal losses Vomiting Diarrhoea Skin losses Respiratory losses

Renal losses Diabetes insipidus Extrarenal losses Vomiting Diarrhoea Skin losses Respiratory losses

Hypertonic saline Sodium bicarbonate Cushings syndrome Hyperaldosteronism

Diagnostic approach to hypernatremia 6. Hypernatremia is serum Na > 145mmol/L. 7. Assess the extracellular fluid (ECF) volume a. Hypovolemia: caused by loss of hypotonic fluids b. Hypervolemia: caused by gain of hypertonic fluids c. Euvolemia: caused by net loss of free water 8. If there is loss of fluids, determine whether the loss is from renal or extrarenal causes. Treatment approach 9. 10. In hypovolemic states, replace extracellular volume deficit with isotonic saline first. Once euvolemia is achieved, calculate the total body water deficit using the formula: TBW = (0.6 x body weight) x [1-(140/current Na)] This deficit may be replaced by hypotonic solutions like 1/2NS, D5% or NG/PO free water. 11. In hypervolemic states, use loop diuretics to remove excess Na. Replace with hypotonic fluids if necessary. 12. Treat underlying conditions e.g. DDAVP for diabetes insipidus. 13. Correction of Na level should be < 1mmol/l/hr for acute & < 0.5mmol/l/hr for chronic hypernatremia, and <15mmol/L in any 8hrs. 14. Avoid overshoot, which can lead to cerebral oedema.

Hyponatremia (Na < 135mmol/L)

Measure plasma osmolality, Posm (Normal 275 to 290mosm/kg)

Normal Posm Hyperlipidemia Hyperproteinemia

Increased Posm Hyperglycemia Exogenous solutes (e.g. mannitol, glycine, glycerol)

Low Posm (True hyponatremia)

Assess ECF volume clinically

Hypovolaemic

Euvolaemic

Hypervolaemic

Urine [Na] <10mmol/L (Extrarenal) GI Losses Skin Losses Third spacing

Urine [Na] >20mmol/L (Renal) Mineralocorticoid deficiency Salt wasting nephropathy Cerebral salt wasting Concurrent diuretic use

Urine [Na] <10mmol/L Congestive cardiac failure Cirrhosis Nephrotic syndrome

Urine [Na] >20mmol/L Renal failure

Measure Urine Osmolality, Uosm

Uosm <100mosm/L (Decreased) Primary polydipsia Profound hypokalemia

Uosm >300mosm/L (Increased)

Uosm variable Pregnancy Reset osmosat

Urine [Na] <10mosm/L Hypothyroidism

Urine [Na] >20mosm/L SIADH Glucocorticoid deficiency Thiazide diuretics

GENERAL ICU CARE


Tracheostomy Change Risk Factors Associated with Difficult Tracheostomy Tube Changes When the stoma is scarred, calcified, distorted or obscured by granulation tissue When the trachea is deviated or rotated When the trachea is narrowed or smaller than normal When the patient is obese If the tube must be placed quickly in an emergency If it is a new or recent tracheostomy within 7 days of insertion If the person performing the change is not well-trained Techniques for a Difficult Trachy Change The obturator helps make insertion easy and trauma-free. Always keep an obturator on hand should the tube need an emergency change. Reposition the patient if needed If the tube cannot be completely inserted, hold the tube in place; remove the obturator to let the patient breath, then continue to insert the tube. If still unable to insert tube, remove the tube, re-lubricate and try again. If this is unsuccessful, try to insert the one size smaller tube. Try spreading the skin around stoma and try to insert tube as the patient is breathing in. If needed, insert a suction catheter through the smaller tube and guide the suction catheter into the trachy stoma. Then slide the trachy tube over the suction catheter and into the stoma. Remove the suction catheter. If all else fails, cut a section of suction catheter to place it into the stoma in order to keep the stoma open and maintain an airway. Be sure to cut the catheter long enough so that it cannot be aspirated! Give supplemental oxygen if needed and available call for senior help! Do not force tube!

Central Line Insertion Good Practice points 1. Seldinger technique is strongly recommended for all CVC insertions, as the size of the needle is smaller, hence accidental arterial puncture is less traumatic. 2. Antimicrobial-impregnated CVC should be used for patient with high risk of septic complication. 3. The procedure must be done under strict aseptic technique. Use maximal sterile barrier precaution during catheter insertion. Use surgical mask, sterile gown, gloves and large sterile drape. GUIDELINES Indications for procedure: 1. Hemodynamic monitoring 2. Total Parenteral Nutrition 3. Emergency haemodialysis 4. Drug administration (e.g. inotropes) 5. Difficult peripheral venous cannulation 6. Long term antibiotics

Contraindications: Relative contraindications may include coagulopathy and central venous thrombosis. Patient with coagulopathy should have fresh frozen plasma or platelet transfusion during CVC insertion. Patient with central venous thrombosis should be referred to radiologist for CVC insertion under ultrasound and fluoroscopic guidance. Insertion Sites 1. Internal Jugular Vein The risk of arterial puncture is significant in internal jugular catheterization. Internal jugular catheterization may be difficult in morbidly obese patients, as the landmarks of the neck are often obscured. Right is preferred as thoracic duct is on the left (Chylous leak). 2. Subclavian Vein Subclavian venous catheterization carries a lower risk of catheter-related infection, thrombosis and arterial puncture. 3. Femoral Vein As the area is near the groin, it has a higher risk of contamination. Although easily accessible, femoral venous catheterization is not recommended for routine central venous cannulation, except in emergencies whereby central venous access is needed for resuscitation from shock. Considerations Patient specifics All patients should be assessed for factors that may increase the risk of catheter insertion: patient anatomy (e.g. morbid obesity, cachexia, anatomic deformity or scars from surgery or radiation treatment), history of failed catheterization attempts or the need for catheterization at a site of previous surgery . Patient setting (e.g. patients receiving mechanical ventilation or during emergencies such as cardiac arrest) co-morbidities (e.g. bullous emphysema, pneumothorax, thrombosis or coagulopathy)
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Operator/Supervisor expertise The operator must have at least 3 successful insertions, supervised by the registrar and above. Seek help early if you suspect it to be a difficult cannulation. Use of Ultrasonic guidance Ultrasonic guidance should be considered in the following situations: Renal patients who have had many previous cannulations and/or thrombosed veins Patients with DIVC or coagulopathy problems. Obese and short neck patients (to include goiter patients). Training of medical staff to confirm surface landmark. PROCEDURE Explain the procedure to the patient. Document patients condition and vital signs. Verify indications and contra indications. Internal jugular vein approach 1. Place patient in slight trendelenburg position (20) with head slightly turned to the contralateral side. 2. Infiltrate local anaesthetic at the junction of the sternal and clavicular heads of the sternocleidomastoid muscle. 3. Insert the needle at an angle of approximately 30 to the skin and again directed toward the ipsilateral nipple. 4. The vessel should be entered within 2-3 cm of insertion. 5. Once vascular access has been obtained, the procedure is repeated with the introducer needle; the guide-wire is passed through the needle and cannulation is completed using Seldinger technique. Subclavian vein approach 1. The patient is propped and positioned in a manner analogous to that for internal jugular vein cannulation. 2. A rolled-up towel however, may be placed longitudinally between the scapulas to allow the shoulders to drop back. 3. The patients head is turned 45 away from the site of the intended placement. 4. The puncture site is identified approximately 1 cm below the inferior margin of the clavicle at the junction of the medial and middle thirds. 5. Infiltration of the region with 1% Lidocaine is accomplished. 6. The anaesthesia needle is removed and the introducer needle is inserted into the skin. The tip is aimed at the suprasternal notch, passing just beneath the clavicle. 7. The bevel of the needle should be pointed towards the leg (caudal). When free flow of blood is obtained from the introducer needle, the guide-wire is inserted and catheter is threaded, the wire removed, fluid flow is established, and the catheter is then secured. Femoral vein approach

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1. This approach is easily performed in most patients. 2. The patient is placed supine, knees extended, and the foot of the anticipated cannulation site is rotated outward at 15-30. 3. The site of insertion is cleaned and prepped, as noted previously, and the region draped. 4. The insertion point is identified, lying 2-3 cm inferior to the inguinal ligament (1-2 cm medial to the femoral pulse). 5. As for internal jugular cannulation, a 23-gauge finder needle is commonly used for local anaesthesia infiltration as well as for localisation of the vessel. 6. After the femoral vein has been found, the introducer needle is placed on a syringe and inserted into the femoral vein. 7. A flexible guide-wire is then placed and the needle exchanged for the vascular cannula. The catheter is then secured. Precautions Guide for length of CVC to be left in-situ is about 12-15 cm, very rarely beyond 15cm. Never force the guide-wire along, as it is most probably not in a vein. Never pull the guide-wire back through needle as it may shear the wire. Never push the guide-wire beyond 20 cm as it may cause arrhythmias. Bilateral attempts cannulation in one sitting should be avoided Never insert the introducer needle beyond 3 cm in IJV approach as the risk of pneumothorax is increased. Do not insert the dilator too deep to cause trauma, it should be just deep enough to facilitate the passage of catheter. Post Procedure 1. Document the date and time of the procedure done. 2. Record the findings of the procedure, the waveform and readings on the monitor scope. 3. Monitor patients condition and vital signs (and O2 saturation when required). 4. Check chest x-ray as soon as possible after CVC insertion to confirm that the tip of the catheter in the superior vena cava and to exclude pneumothorax / haemothorax. 5. Observe patient for possible complication such as: Pnemothorax Haemothorax Haematoma Arterial Puncture Infection Chylothorax Arrhythmia Thrombosis Air Embolism Cardiac Tamponade

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6. All CVC should be reviewed daily, to decide on the need for: Removal, re-insertion, if suspected of sepsis or patient still required it Change of CVC Whenever there is evidence or suspicion of an infected CVP line, the catheter should be removed immediately under sterile conditions. Always suspect CVP lines to be sources of infection, when there is redness/pus around CVP wound site. Patient is febrile with evidence of infection but all other sources have already been excluded. Steps to be taken if patient has clinical evidence of infection: Obtain blood culture taken from a peripheral venepuncture site. Two sets of blood culture will give a better yield of results than one (one set refers to sample taken from one site for both aerobic and anaerobic culture; a second set should be taken from another site about one hour later).If catheter is to be removed, cut off the 5cm distal tip with a sterile pair of scissors. Place the specimen in a sterile specimen container and send to Microbiology Laboratory as soon as possible to prevent drying. Any CVC placed with non-sterile technique, such as one placed on an Emergency basis during resuscitation efforts or trauma, should be changed when the patient is stabilized. Removal of CVC 1. Place patient in trendelenburg position. 2. Cleanse the insertion site with 70% ethyl or isopropyl alcohol. Allow to site to dry. 3. Remove any anchoring stitch if present. Place gauze over the puncture site, gently remove the catheter and apply pressure for 5 minutes. 4. After bleeding has stopped, spray Opsite and apply a light dressing. 5. Send the catheter tip for culture only when clinically indicated. Do not send for routine surveillance culture.

INOTROPES AND VASOPRESSORS


HO VUI KIAN Inotropes and Vasopressors are agents often used in hypotension and shock. In general, inotropes augment cardiac contractility, thus improving cardiac output with the aim of improving organ perfusion. Vasopressors may improve perfusion by increasing SVR, thereby improving MAP and hence organ perfusion pressure. Most agents have a combination of both inotropic and vasopressive effects, in varying proportions. Its use in hypotension and shock is often as a temporizing measure, and not a cure. It is crucial to identify the cause of the hypotension and treat it. Remember inotropes are not a substitute for fluid loading in hypovolemic patients. As far as possible, all inotropes (with the exception of dopamine) should be infused through a central venous catheter. Common Inotropes Adrenaline (Epinephrine) Use: Inotropic support, Cardiopulmonary collapse (ACLS), Cardiogenic shock, Bronchospasm, Anaphylaxis Dose: Anaphylaxis: IM/SC 0.1-0.5mg q10min till improvement or IV 0.1-0.25mg over 5min, repeat q5-15min or infusion 1-4 mcg/min Bronchodilation: IM/SC 0.1-0.5mg ACLS: 1mg (in 10ml) q3-5 min. High dose therapy: 0.1mg/kg Hypotension: IV infusion 0.01-0.2 mcg/kg/min Mechanism: low dose 1 (inotropic) & some 2 (vasodilation - muscles), 1 (vasoconstriction skin/ kidney/ splanchnic); moderate dose primarily 1; high dose primarily 1. CVS Effects: HR, SV, CO , SBP (MAP ), SVR +/Adverse Effects: Tachycardia, Arrhythmias, Hyperglycemia, Hypokalaemia (exacerbated by insulin started for hyperglycemia), Lactate , Renal perfusion , Myocardial ischemia Elimination: Hepatic Half life: < 1 min Noradrenaline (Norepinephrine) Use: Severe hypotension due to distributive shock/ SVR (1st line for septic shock); Inotropic support, Hypertensive Therapy (HHH) Dose: IV infusion 0.01-0.02 mcg/kg/min (max 1 mcg/kg/min) Mechanism: Primarily 1 effects CVS Effects: HR , SV , CO +/-. SBP (MAP), SVR . Adverse Effects: Reflex bradycardia, Ischemia/ gangrene of any end organ, renal perfusion , Arrhythmias Elimination: Hepatic Half life: < 1min Dopamine Use: Inotropic support (Cardiogenic/ Septic shock) Dose: IV infusion 1-20 mcg/kg/min Mechanism: Low dose via DA receptors, moderate dose via 1, high dose via 1 CVS effects: Low dose 1-5 mcg/kg/min renal perfusion, minimal BP effects (but renal dose to increase urine output/ maintain renal function has been disproved) Moderate dose 5-15 mcg/kg/min SV, CO, HR High dose > 15mcg/kg/min SVR , HR with BP

Adverse Effects: Tachycardia, arrhythmias (high doses), ischemia/ gangrene (high dose) Elimination: Hepatic Half life: 2 min Onset: <5 min Vasopressin Use: Septic Shock (adjunct), Cardiopulmonary collapse (ACLS alternative to adrenaline), Diabetes insipidus, GIT bleeding Dose: Diabetes Insipidus: IM/SC 5-10 units bd-qds GIT bleeding: IV 20 units over 15min then infusion at 0.2-0.4 units/min (max 0.9 units/min) ACLS: IV 40 units bolus (once only) Septic shock: 0.01- 0.05 units/min (Max 0.1 units/min) Mechanism: V1 (vasoconstriction), V2 ( water permeability of renal tubules) CVS Effects: SVR , SBP/ MAP , HR , CO +/Adverse Effects: AMI/ ischemia/ gangrene (high doses) Elimination: Hepatic and renal Half life: 10-20min Onset: minutes Dobutamine Use: Cardiac inotropic support (virtually pure adrenergic agonist) Dose: 1-20 mcg/kg/min (Max 40 mcg/kg/min) Mechanism: 1 up to 10mcg/kg/min; 2 vasodilation > 10mcg/kg/min CVS Effects: HR, SV, CO , SBP/MAP or, SVR Adverse effects: Tachycardia, hypotension (with higher dose) Elimination: Hepatic Half life: 2 min Onset: 1-2 min

Anaphylaxis
Recognition of anaphylaxis Anaphylaxis is a sudden catastrophic allergic reaction that involves the whole body. It usually occurs within minutes of exposure to the offending allergen (insect stings, nuts and medicines being the commonest causes). Anaphylaxis is typically rapid and unpredictable with variation in clinical presentation. The most common features include: Cardiovascular collapse Bronchospasm difficulty in breathing which often presents as noisy breathing Angioedema swelling of mucous membranes and tissues beneath the skin Pulmonary oedema deposit of fluid into the lungs Loss of conciousness Urticaria Itchy skin eruptions characterised by weals with pale interiors and well defined red margins

Frequency of Signs and Symptoms

Signs and symptoms Urticaria, angioedema Dyspnea, wheeze Dizziness, syncope, hypotension Nausea, vomiting, diarrhea, cramping abdominal pain Flush Upper airway edema Headache Rhinitis Substernal pain Pruritus without rash Seizure

Frequency (%) 88 47 33 30 46 56 15 16 6 4.5 1.5

Protocol for Treatment of Anaphylaxis 1. Diagnose the presence or likely presence of anaphylaxis. 2. Place patient in recumbent position and elevate lower extremities. 3. Monitor vital signs frequently (every two to five minutes) and stay with the patient. 4. Administer epinephrine 1:1,000 (weight-based) (adults: 0.01 mL per kg, up to a maximum of 0.2 to 0.5 mL every 10 to 15 minutes as needed; children: 0.01 mL per kg, up to a maximum dose of 0.2 to 0.5 mL) by SC or IM route and, if necessary, repeat every 15 minutes, up to two doses). 5. Administer oxygen, usually 8 to 10 L per minute; lower concentrations may be appropriate for patients with chronic obstructive pulmonary disease. 6. Maintain airway with an oropharyngeal airway device. 7. Administer the antihistamine diphenhydramine (Benadryl, adults: 25 to 50 mg; children: 1 to 2 mg per kg), usually given parenterally. 8. If anaphylaxis is caused by an injection, administer aqueous epinephrine, 0.15 to 0.3 mL, into injection site to inhibit further absorption of the injected substance. 9. If hypotension is present, or bronchospasm persists in an ambulatory setting, transfer to hospital emergency department in an ambulance is appropriate. 10. Treat hypotension with IV fluids or colloid replacement, and consider use of a vasopressor such as dopamine (Intropin). 11. Treat bronchospasm, preferably with a beta II agonist given intermittently or continuously; consider the use of aminophylline, 5.6 mg per kg, as an IV loading dose, given over 20 minutes, or to maintain a blood level of 8 to 15 mcg per mL. 12. Give hydrocortisone, 5 mg per kg, or approximately 250 mg intravenously (prednisone, 20 mg orally, can be given in mild cases). The rationale is to reduce the risk of recurring or protracted anaphylaxis. These doses can be repeated every six hours, as required. 13. In refractory cases not responding to epinephrine because a beta-adrenergic blocker is complicating management, glucagon, 1 mg intravenously as a bolus, may be useful. A continuous infusion of glucagon, 1 to 5 mg per hour, may be given if required. 14. In patients receiving a beta-adrenergic blocker who do not respond to epinephrine, glucagon, IV fluids, and other therapy, a risk/benefit assessment rarely may include the use of isoproterenol (Isuprel, a beta agonist with no alpha-agonist properties). Although isoproterenol may be able to overcome depression of myocardial contractility caused by beta blockers, it also may aggravate hypotension by inducing peripheral vasodilation and may induce cardiac arrhythmias and myocardial necrosis. If a decision is made to administer isoproterenol intravenously, the proper dose is 1 mg in 500 mL D5W titrated at 0.1 mg per kg per minute; this can be doubled every 15 minutes. Adults should be given approximately 50 percent of this dose initially. Cardiac monitoring is necessary and isoproterenol should be given cautiously when the heart rate exceeds 150 to 189 beats per minute.

Sedation in the Intensive Care Unit


Zheng Jin Xi

Indications

Reduce discomfort / anxiety / restlessness / agitation Improve tolerance to ICU procedures Ameliorate stress response Facilitate endotracheal tube tolerance, ventilator synchrony Prevent awareness during neuromuscular paralysis

Complications

Accumulation with prolonged infusion Delayed weaning from supportive care Detrimental effects on circulation Tolerance and withdrawal Venous thrombosis from decreased mobility Reduced intestinal motility Inability to assess neurological status effectively during sedation

Assessment of depth of sedation

Ramsay Sedation Scale Score Response 1 Awake, anxious, agitated or restless 2 Awake, cooperative, orientated, tranquil 3 Drowsy, responds to verbal commands 4 Asleep, brisk response to glabellar tap or loud auditory stimulus 5 Asleep, sluggish response to glabellar tap or loud auditory stimulus 6 Asleep, no response

Sedation target: 2-3 during daytime to accommodate clinical assessment, family visits
4-5 during night or painful procedures

Vital signs (useful in deep sedation or concomitant neuromuscular blockade) Heart rate Blood pressure

Drug Propofol

Dose
Loading dose 550mg Maintenance infusion 0.54mg/kg/hr

Pros
Fast onset Fast offset after infusion ICP reduction Anticonvulsive activity Elimination not impaired in liver cirrhosis or renal insufficiency Fast onset Short duration of action Less hemodynamic compromise Amnesic effect Presence of reversal agent

Cons
Hypotension Bradycardia Respiratory depression Hyperlipidemia Pain on peripheral administration No analgesic effect Propofol infusion syndrome Accumulation with prolonged infusion Respiratory depression Decreased clearance in hepatic or renal dysfunction Tolerance and withdrawal No analgesic effect Hypotension Bradycardia Respiratory depression Histamine release Nausea Constipation Prolonged sedation in renal insufficiency Bradycardia Hypotension Transient hypertension on rapid administration Rebound hypertension on rapid withdrawal Nausea Limited clinical experience

Remarks
Propofol infusion syndrome: Rare, often fatal Described in critically-ill children on high dose longterm propofol infusion Features include cardiac failure, rhabdomyolysis, severe metabolic acidosis, renal failure Risk increases with doses >4mg/kg/hr for 48 hours

Midazolam

Loading dose 2-4mg Maintenance infusion 0.5-10mg/hr

Morphine

Loading dose 25mg Maintenance infusion 1-5mg/hr

Analgesic Antitussive Fast onset Presence of reversal agent

Dexmedetomidin e

Loading infusion 1mcg/kg over 10min Maintenance infusion 0.20.7mcg/kg/hr

Analgesic sparing activity Patients sedated when undisturbed but arouse readily with gentle stimulation Respiratory stability

Approved only for short term use (<24hrs) for sedation in the intensive care setting

Flumazenil (Anexate) Competitive antagonist of BDZ; must accompany pt if sedation is given Onset 2mins after IV, peak in 10 mins Initial dose 1mg, then titrated to effect 0.2mg increments. Caution in pts with long term BDZ therapy. Seizures may occur. Naxolone Competitive antagonist of opioids; must accompany pt if sedation is given Rapid onset, duration of action is dose-related. Max 2mg Initial doses 0.4mg IV. Dilute this to 10mls and give 1ml (0.04mg) at a time. Acute reversal of opioid can cause pain, hypertension, tachycardia and pulmonary edema

Establish sedation goal

Is the patient comfortable and at desired sedation goal?

No

Yes

Identify and treat any underlying physiological disturbances first


Hunger, thirst, constipation, full bladder, hypoxemia, hypoglycemia, hypotension, pain, drug withdrawal

Sedation algorithm

Frequent assessment of depth of sedation Review sedation goal daily

Non-pharmacologoical measures

Reassurance, frequent reorientation, proper positioning, maintenance of patient comfort, and optimization of the environment (eg humidity, lighting, temperature, noise)

Yes

Is the patient comfortable and at desired sedation goal?

Analgesia as initial therapy

If pain is the suspected cause of agitation

No

Yes

Administer sedative infusion


Sedative dosage should take into account level of sedation required, and patient factors affecting drug clearance Loading dose titrated to effect followed by a maintenance infusion To increase sedation, give small bolus followed by small increment in infusion rate Combinations of sedatives can have synergistic effects, can be more effective than single sedative at high dose

Consider drop in infusion rate


To decrease sedation, stop infusion then restart at lower rate when appropriate level of sedation reached

Consider sedative withdrawal Potential for effects of opioid, benzodiazepine, and propofol withdrawal should be considered after high doses or more than approximately seven days of continuous therapy Doses should be tapered systematically to prevent withdrawal symptoms

Consider sedation holiday

Daily interruption of infusion, allowing patient to wake Infusion should be restarted once the patient is fully awake and obeying commands or until they became uncomfortable and require the resumption of sedation Advantages Decreases days of mechanical ventilation and length of ICU stay Minimizes complications of sedation, reduces tendency for drug accumulation Facilitates neurological assessment and communication with patient

Blood Sugar control


Chen Xuan Xuan Hyperglycemia and insulin resistance are common in critically ill patients, even when glucose homeostasis has previously been normal. Contributing factors include stress, use of glucocorticoids, use of inotropes eg. adrenaline Strict glycemic control (glucose level 4-6mmol/L) reduces morbidity and mortality Morbidity reduction in terms of: a) critical illness polyneuropathy b) bacteremia c) red cell transfusion d) inflammation e) acute renal failure f) duration of mechanical ventilation Despite need for glycemic control to reduce morbidity and mortality, risks of hypoglycemia with insulin regime should not overlooked. Issue of hypoglycemia early hypoglycemic symptoms not easily recognized in critically ill patients severe hypoglycemia (glucose <1.7mmol/L) or prolonged hypoglycemia can lead to convulsions, coma, irreversible brain damage and cardiac arrhythmias importance of close blood glucose monitoring and titration of insulin dose, especially if feeding is interrupted eg. Preparation for extubation, transportation for surgery, procedure

Insulin regime Commonly as intravenous infusion of insulin through a central venous catheter.

Surgical Nutrition Estimation of caloric and protein requirements is necessary to provide adequate substrates for healing and tissue repair. Failure to provide adequate amounts of both calories and protein leads to further depletion of lean body mass. Basal energy expenditure (BEE) can be predicted using the Harris-Benedict equation:
BEE (kcal/day), men = 66.4 + (13.7 weight in kg) + (5.0 height in cm) (6.7 age) BEE (kcal/day), women = 655 + (9.6 weight in kg) + (1.8 height in cm) (4.7 age)

These equations provide a reliable estimate of the energy requirements in approximately 80% of hospitalized patients. The actual caloric needs may be substantially greater than the BEE during periods of metabolic stress Most stressed patients require 2535 kcal/kg per day. Metabolic activity factor(MAF) MAF = Activity factor + Injury factor + Growth factor Activity factor Injury factor Bedrest 0.2 Minor surgery 0.2 Moderately active 0.35 Major surgery 0.35 Active 0.5 Major burns 1.0

Growth factor Moderate wt loss 0.05 Severe wt loss 0.13

After craniotomy :26/kcal/kg/day GCS 4-5 : 50kcal/kg/day GCS 6-7: 40kcal/kg/day GCS 8-12 : 35kcal/kg/day Fever : BEE x 1.1( for each C above body temp) BEE is increased by 40% for 3 weeks after HI; Stroke pts BEE increased by 20% Paraplegia pts : 23kcal/kg/day Quadrplegia: 27kcal/kg/day Brain death pts: 10kcal/kg/day Actual Energy Expenditure(AAE) AAE = BEE x [ metabolic activity factor(MAF) + 1.0] Protein Requirements and Nitrogen balance Protein 0.8-2.0g/kg per day 1g N2 = 6.25g protein

Principles of Surgical Nutrition 1. Most surgical patients do not require nutritional supplementation and has adequate reserves to withstand common catabolic stresses and partial starvation for a week.; IV fluids with adequate electrolytes with a min of 100mg of glucose/day is adequate(to minimise protein catabloism) 2. Enteral nutrition is preferable over parenteral as it simple, physiological , safe and cheap. It indicated in pts who cannot maintain an adequate oral intake but has a function GIT. Refer to Dietician for optimisation. Nutritional Assessment 1. History: Dietary habits, anorexia, loss of weight( 5% over 1/12, or 10% over 6/12 is significant); current medications 2. Physical examination

a. Muscle wasting, Weight, Height, BMI b. Signs of nutritional deficiencies skin rash pallor, glossitis, hair changes, neuropathy c. Anthropometry measurementstriceps skinfold, midarm circumference 3. Laboratory indicators a. Serum Alb(<35mg/dl), serum transferrin(<200mgl/dL) b. Serum prealbumin(<17mg/dL:mild,<10:moderate,<5: severe) c. Total Lymphocyte count : % Lymphoctyes x TW/100 i. 1500-1800 mm3 : mild depletion ii. 900-1500 mm3 : moderate depletion iii. <900 mm3 : severe depletion Nutritional support should be initiated in the followings: patients who have inadequate oral intake for 7 days, patients in whom inadequate oral intake is expected to last for at least 7 days period. In general, enteral nutritional support should be used in preference to parenteral nutrition to provide nutritional support to patients with functioning gastrointestinal tract but who are unable to meet their nutritional requirements on their own. Early enteral nutrition should be considered for critically ill with functioning gut and postoperative colorectal surgery patients. Access for enteral nutrition: 1. Patients with neurologic dysphagia or those who need enteral nutritional supplementation can be fed through nasogastric tubes. 2. Patients at high risk of aspiration due to mental obtundation, gastroparesis or incompetent lower oesophageal sphincter should be fed through the naso-jejunal routes. 3. Percutaneous endoscopic gastrostomy (PEG) or surgical jejunostomy PEG can be used as long term enteral feeding access for patients who have been unable to feed orally for more than 6 weeks and have anticipated life expectancy of more than 6 months. Contraindications to enteral feeding are as follows: 1. Mechanical bowel obstruction 2. High output, proximal bowel fistula (>200ml/day) 3. Severe malabsorption 4. Short bowel syndrome in early phase Parenteral nutrition should be used when: 1. the gastrointestinal tract is not functional 2. the gastrointestinal tract cannot be accessed 3. patients cannot be adequately nourished by oral diets or enteral nutrition. The use of parenteral and enteral nutritional support should not be considered in exclusion of one another for critically ill patients. Parenteral nutritional support can be given to critically ill patients with ileus / gastroparesis, and enteral nutrition through nasogastric (or preferably nasojejunal tubes) should also be initiated at low rates simultaneously with the assistance of pro-motility agents (intravenous metoclopramide), if required.

Preoperative nutritional support is indicated in severely malnourished patients undergoing major gastrointestinal tract surgery. It should be administered for 7-14 days if surgery can be safely postponed for this period. Postoperative parenteral nutrition should not be routinely given in the immediate postoperative period. It should be administered to patient who is malnourished and/or is anticipated not to be able to meet their nutritional needs (orally / enterally) for at least 7 days period. Disease-specific formulae use should be restricted only to patients who are unable to tolerate standard polymeric diets. The exception will be patients with chronic renal failure who need electrolytes and fluid restriction. For end stage renal disease (ESRD) patients who have inadequate intake, fortified oral diet with energy and protein supplement should be initiated. If oral nutrition (including nutritional supplement) is inadequate, enteral tube feeding should be considered. For those who do not tolerate tube feeding, intradialytic parenteral nutrition (IDPN) may be considered for haemodialysis patients and intraperitoneal nutrition (IPN) for continuous ambulatory peritoneal dialysis (CAPD) patients. Currently, TPN bags are available in two forms: hospital compounded (HC) bags which are prepared according to patients specific needs by hospital compounding units or commercially available Ready-to-use (RTU) bags. Patient who can be considered for RTU are those who do not have impairment of renal function, gross disturbances in electrolyte, short bowel syndrome, high output fistulae or risk of refeeding syndrome. To prevent inappropriate use of TPN, RTU should be made available ONLY upon referral to the Nutritional Support Service, except in SICU.
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Oxygen Therapy Indications 1. Cardiac and/or respiratory arrest 2. Hypoxaemia (PaO2 < 60 mmHg, SaO2 < 90%) 3. Hypotension (Systolic blood pressure < 100 mmHg) 4. Low cardiac output and metabolic acidosis (Bicarbonate < 18 mmol/L) 5. Respiratory distress (respiratory rate > 24/min) 6. An acute care situation in which hypoxaemia is suspected 7. Short-term therapy (e.g., post-anaesthesia recovery) SUGGESTED INITIAL OXYGEN DOSE Condition Other acute conditions (e.g., asthma, pulmonary embolus) Hypoxaemia with PaO2 < 40 mmHg Chronic obstructive lung disease patients with hypoxaemia and PaCO2 > 40 mmHg FiO2 (%) 60 100 % 40 60 % 24 28 %

Need is determined by measurement of inadequate oxygen tensions (PaO2) and/or saturations (SaO2/SpO2) by invasive or non-invasive methods. OXYGEN DELIVERY EQUIPMENT Low-Flow Systems Low-flow systems deliver 100% oxygen at flows that are less than the patients inspiratory flow rate (i.e., the delivered oxygen is diluted with room air). Thus, the oxygen concentration inhaled (FiO2) may be low or high, depending on the specific device and the patients ventilatory pattern (e.g., minute volume, respiratory rate or inspiratory flow rate).
Equipment Nasal cannula Litre Flow 1 6 LPM % O2 Delivered 24 40 % Comments delivers approximately 4% per litre above room air, i.e., 21% humidification not required when using flowrates of 1 4 LPM patent nasal passages required flowrates > 5 LPM are needed to avoid rebreathing exhaled CO2 flow should be sufficient to reservoir bag inflated during inspiration higher FiO2 is possible depending on mask fit and ventilatory pattern

Simple mask Non-breathing mask (NBRM)

5 10 LPM 6 15 LPM

35 50 % 60 % ++

High-Flow Systems

High-flow systems can accurately deliver predetermined oxygen concentrations of up to 40% to the trachea by exceeding the patients inspiratory flowrate and minute volume. The precise concentration of oxygen delivered by a venturi is achieved in one of two ways: i. ii. using individual, but different size jets with a fixed entrainment port, or using a single jet with an adjustable entrainment port or dilutor valve.

Equipment
Venturi Mask (Individual Jets)

Venturi Mask (Adjustable Diluter Valve)

High Volume Nebulisers Ohio)

Oxygen Litre Flow 2 LPM (Blue) 4 LPM (Yellow) 6 LPM (White) 6 / 8 LPM 8 LPM (Pink) 12 LPM (Orange) 6 LPM (White) 3 LPM (White) 6 LPM (White) 6 LPM (White) 9 LPM (Green) 12 LPM (Green) 15 LPM (Green) 10 LPM 10 LPM 10 LPM

Total Flow 52 LPM 50 LPM 54 LPM 36 48 LPM 32 LPM 32 LPM 79 LPM 47 LPM 68 LPM 53 LPM 50 LPM 50 LPM 41 LPM 40 LPM 20 LPM 10 LPM

Oxygen (%) 24 % 28 % 31 % 35 % 40 % 50 24 % 26 % 28 % 30 % 35 % 40 % 50 40 % 60 % 100

% %

MONITORING Clinical assessment including cardiac, pulmonary, and neurologic status. Assessment of physiologic parameters : measurement by arterial blood gases or noninvasively by pulse oximetry in patients treated with oxygen.

Eye Care Guidelines

Maintain the integrity of the ocular surface and prevention of ocular complications which includes: Corneal ulcer Bacterial keratitis Corneal abscess Corneal abrasion The nurse performs eye toilet and inspects the patients eyes at least once per shift and whenever necessary. Assess and document the degree of eye closure/corneal exposure in the progress notes. Initiate appropriate prophylactic treatment as suggested below.The assessment and documentation will be based on the following table on Grading of Eye/Corneal Exposure
Grade Grade 1 Grade 2 Degree of Eye/ Corneal exposure Patients lids are completely closed with no visible gap between eyelids Lids are apart, and conjunctiva exposed (white of the eye is visible) Grade 3 Lids are apart, and the cornea exposed Prophylactic intervention No treatment necessary Apply lubricants every 4 hours. Suggested lubricative ointment e.g. Duratears or Lacrilube Horizontal lid taping using Micropore tape (ensure full eyelid closure beneath the tape) Grade 4 Patient ventilated in a prone position & Apply lubricants every 4 hours. Horizontal lid taping using Micropore tape ( ensure ful eyelid closure beneath the tape ) & Apply lubricants 4 hourly.

Assess need for ophthalmology referral:When suspect: Corneal ulcer Bacterial keratitis Corneal abscess Corneal abrasion Conjunctival abrasion Signs presence of sticky mucoid or mucopurulent discharge or crusting around eyelids red, inflamed eyes presence of a visible corneal epithelial defect or ulcer presence of white corneal lesions When patient is unable to maintain full closure of eye and if tarsorraphy is indicated. Deep Vein Thrombosis Patients must be routinely screened and risk-stratified for clinical risk factors and overall risk of venous thromboembolism. Patients who are identified to be at risk of developing venous thromboembolism should be given thrombo-prophylaxis, i.e. specific

anti-thrombotic drugs with or without mechanical devices to reduce the risk of deep vein thrombosis, pulmonary embolism, and possible fatality. Based on the Scottish Intercollegiate Guidelines Network (SIGN), patients at risk for developing venous thromboembolism are classified into the following groups:
Low Risk Group Absence of thrombophilia and diseases associated with hypercoagulable states Absence of other risk factors Minor surgery, trauma or medical illness at any age Major surgery age under 40 years. Moderate Risk Group Absence of thrombophilia and diseases associated with hypercoagulable states All major surgery with presence of other risk factors Minor surgery in patients with previous history of DVT/PE. High Risk Group Major surgery in patients with single or recurrent previous DVT/PE Family history of DVT/PE Presence of thrombophilia and diseases associated with hypercoagulable states Fractures involving pelvis, hip, lower limbs Major surgery involving pelvis, hip, lower limbs Major cancer surgery.

GUIDELINES Identification of patients meeting specific prophylaxis All medical and surgical patients admitted to hospital, as well as all pregnant or puerperal women, must be routinely assessed for clinical risk factors and overall risk of venous thromboembolism. Patients who require thrombo-prophylaxis and recommended interventions : Surgical patients for elective major surgery and medical patients with prolonged immobilisation (above 4 days) Early mobilisation with or without compression stockings should be considered for the following patients: Absence of past history and family history of venous thrombosis; Absence of thrombophilia and diseases associated with hypercoagulable states; Less than 4 other risk factors for DVT. Pharmacologic peri-operative prophylaxis should be indicated for patients with: Presence of thrombophilia and diseases associated with hypercoagulable states Past history and family history of venous thrombosis 4 or more other risk factors for DVT Methods of prophylaxis Mechanical methods Graduated compression stockings(T.E.D) and intermittent pneumatic compression devices should be considered for DVT prophylaxis in moderate risk surgical patients. They do not increase the risk of bleeding and can be safely used in patients with high-risk of bleeding. These devices are contraindicated in patients with severe leg ischaemia. Pharmacological methods for Surgical and Medical patients

Unfractionated Heparin, Low Molecular Weight Heparins, Warfarin, Dextran are useful in preventing DVT/PE. However the use of Low Molecular Weight Heparins are highly efficacious with less bleeding complications. It is easy to administer and in most cases monitoring of clotting times is not required. Low molecular weight heparin regimens: Fraxiparine - 0.2 ml daily if bodyweight < 50 kg, 0.3 ml daily if bodyweight > 50 kg till fully mobilised. Clexane - 20 mg daily till fully mobilised. Contraindications to pharmacological thrombo-prophylaxis Patients with known bleeding disorders e.g. haemophilia, Von Willibrand's Disease, thrombocytopenias and platelet dysfunction Acquired coagulopathy secondary to liver diseases, drugs, uraemias, etc Strong family history of bleeding disorders Underlying pathology which predispose to bleeding, e.g. peptic ulcers, haemangiomas Neuro-surgery and eye surgery. However, for those patients with very high risk of thrombosis, pharmacological thrombo-prophylaxis should be considered a few days after the surgery when there is reduced risk of bleeding and before the patient is ambulant.

Pulmonary embolism Pulmonary embolism is a feared, sometimes fatal event, which rarely occurs as an isolated incident. Pulmonary embolism is a clot found in the peripheral vein, which travels through the central vein circulation to lodge in the pulmonary arterial tree. History and physical examination All patients suspected of having suffered a pulmonary embolism require a history and physical exam. The history should include, at a minimum, an account of the symptoms, the presence of any risk factors for PE such as advance age, obesity, immobilization, major trauma or surgery, hypertension, diabetes, hyperlipidemia, inherited thrombophilias, pregnancy and puerperium, and the presence or absence of any confounding diagnosis, such as congestive heart failure or chronic obstructive pulmonary disease. In addition, the patients medication should be recorded. The physical examination should include vital signs (blood pressure, pulse, respiratory rate, temperature, and pulse oximetry), an examination of the head and neck including an assessment of neck veins, an examination of chest, and examination of extremities for cyanosis and edema. The calves and thigh should be examined for evidence of deep vein thrombosis. Laboratory and X-ray

FBC, PT/PTT, U&E, ABG. In addition, ECG and CXR Pretest probability for P.E The pretest probability of PE can be estimated by using the Wells et al criteria derived from a thromboembolism referral center in Canada (Table 1).
Table 1. Wells et al criteria for assessment of pretest probability for PE Criteria Clinical signs and symptoms of deep vein thrombosis (DVT) P.E as likely or more likely than an alternative diagnosis (based on history and physical exam, chest radiology, ECG, and any blood tests that are considered necessary) Heart rate >100 beats per min Immobilization or surgery in the last 4 wks Previous DVT/P.E Hemoptysis Malignancy ( on treatment, treated in the past 6 months or palliative Total points Risk score interpretation: <2 points : Low risk , less than 10% probability of PE 2-6 points: Moderate risk; The intermediate-risk patients had a 20-40% range probability of PE >6 points : High risk; a greater than 65% probability of PE Poi nts 3.0 3.0 1.5 1.5 1.5 1.0 1.0

Initial diagnostic test and follow on Available diagnostic tests for PE are pulmonary angiography, spiral CT thorax, ventilation-perfusion lung scan (V/Q scan) and D-Dimer. The standard criterion for the diagnosis or exclusion of P.E remains the pulmonary angiogram. However, the pulmonary angiogram has many drawbacks as a primary screening test for P.E, it has an associated mortality of 0.5%. Currently, the pulmonary angiogram is usually reserved for difficult cases where other screening tests have yielded indeterminate or conflicting information.

Diagram 1.

Pulmonary Embolism Diagnosis Algorithm


Suspected Pulmonary embolism

Clinical Assessment of PE probability

Low

Moderate

High

D-Dimer

-ve

+ve

Spiral CT Thorax

PE excluded

+ve

-ve

PE diagnosed

If clinical suspicion still high

PE excluded

Duplex Ultrasound both lower limbs

-ve

+ve

PE excluded

Treat as for PE

Diagram 2. CT Thorax

Diagnosis Algorithm For Patients Who Cannot Undergo Spiral


Suspected Pulmonary embolism

Clinical Assessment of PE probability

Low

Moderate

High

D-Dimer

-ve

+ve

Ventilation-Perfusion Lung Scan

PE excluded

High-probability V/Q Scan

Non diagnostic

Normal

PE diagnosed

Ultrasonography of proximal limbs

PE excluded

-ve

+ve

Ultrasonography of lower limbs after 1&2 weeks

PE diagnosed

-ve

+ve

PE excluded

PE diagnosed

Indications for Use The monitor is intended for use in monitoring the hypnotic state of the brain by data acquisition of EEG signals of the anaesthetized or sedated patient in all areas of the hospital. The monitor is a non-invasive measurement tool to be used by a trained professional to measure the level of consciousness during general anaesthesia and sedation by use of variations in the frequency content of the spontaneous EEG. It analyses the frequency shifts that take place in the EEG signal as the level of consciousness changes. Based on this principle, the monitor calculates the Cerebral State Index (CSI), which is used to estimate the level of consciousness of the patient.

CSI Scale The CSI is a unit-less scale from 0 to 100, where 0 indicates a flat EEG and 100 indicates EEG activity corresponding to the awake state. The range of adequate anaesthesia is designed to be between 40 and 60. All values in the table are approximate values based on the mean values of the patient behaviour. The relationship between the CSI, the clinical state and the OASS1 score is shown in the table below: The OASS score correspond to: OASS Clinical State 5 Responds readily to name spoken in normal tone 4 Lethargic response to name spoken in normal tone 3 Responds only after name called loudly and/or repeatedly 2 Does not respond to mild prodding or shaking 1 Does not respond to noxious stimulus

CSI 90100

Clinical state awake

OASS 5 4 3 2-1 1 <1

80-90 drowsy 60-80 Light anaesthesia or sedation 40-60 Range considered as adequate for surgical anesthesia 10-40 Deep anesthesia, in most cases accompanied by burst suppression 0-10
Close to coma, BS (burst suppression) larger than 75. When CSI is below 3, the EEG is practically iso-electric

EMG High levels of facial muscular or electromyographic (EMG) activity can interfere with the CSI under certain circumstances. The monitor incorporates an EMG filter that removes most of the potential interfering EMG activity. The EMG bar shows the energy of the EMG level in the 7585 Hz frequency band (0100 logarithmic). The bar is located on the right side of the display. EMG activity is expected to be present when the patient is awake. When the patient is asleep, EMG activity can increase due to: Reflex reactions to painful stimuli during surgery Lack of muscular relaxation Muscular rigidity caused by some opioids (analgesics) Presence of large external electrical fields, e.g. diathermy The EMG bar should be checked frequently, especially in case of a sudden increase in the CSI. If the increase in CSI is accompanied by an increase in muscular activity, there is a risk that EMG is causing interference. When this happens,

attention must be paid to the stimuli received by the patient during surgery. In the presence of hypnotically unrelated EMG, administration of a neuromuscular blocking agent will cause the CSI to decrease. Since patients receiving neuromuscular blocking agents cannot exhibit movement as a sign of arousal, the CSI is a valuable tool in their anaesthetic management. Burst Suppression Indicator The monitor includes a Burst Suppression indicator to show periods when the EEG is iso-electric or flat. The indication appears in the upper left-hand side of the graph window in the display and shows the percentage of burst suppression over the last 30 seconds of the EEG signal. A BS% = 20 readouts means that the EEG has been iso-electric during 20% of the last 30 seconds. Artefact and Noise Control The artefact rejection algorithm ensures that the incoming EEG is not contaminated with noise. When excessive noise is detected, the signal quality index is reduced reflecting the disturbance. The artefact rejection algorithm will be active especially when diathermy and equipment creating external interference is used.

Neuropharmacology
Analgesia Mild pain Generic Name Paracetamol Paracetamol + Orphendarine Hyoscine Fastum gel/ Voren gel Mild to moderate pain Generic Name Proprietary Name Diclofenac Voltaren Indomethacin Mefenamic acid Naproxen Na Piroxicam Codeine Phosphate Tramadol Indocid Ponstan Synflex Feldene Codeine Ultram

Proprietary Name Panadol Anarex Buscopan

Typical adult dosage 1gm PO 4 to 6hrly 1-2 tabs QDS PO 10-20mg TDS PO 20mg(1ml) IM Topical rub

Max dose/day 4000mg 8 tabs

Notes Hepatoxicity Muscle relexant for colic MSK pain

Typical adult dosage 25-50 mg PO TDS 25-50mg TDS PO 250-500mg TDS 550mg BD PO 10-20mg QDS PO 30-60mg QDS to Q3/PRN IM/PO 50-100mg TDS /QDS/PRN PO

Max dose/day 150mg 200mg 2000mg 1375mg 100mg 480mg 400mg

Notes NSAIDs NSAIDs NSAIDs NSAIDs NSAIDs Weak opioid Opioid

NSAIDs : Opioids : effects

Need to add Famotidine 20mg BD PO or Losec 20 mg BD PO for gastric protection Need to add lactulose 5-10 mls TDS PO, Senna 1-2tabs ON PO to prevent constipation, add Maxalon 10mg BD/TDS IM/PO for antiemetic Typical adult dosage 5-15mg Q4-6 PO 1-10mg Q4-6 SQ, 0.5-2mg/hr IV 25 to 75mg TDS Max dose/day For IV,need monitoring Notes Consult with senior if in doubt Add maxalon

Severe Pain Proprietary Name Mist Morphine oral M Subcutaneous orphine Intravenous Generic Name Pethidine Intramuscular

PRN IM 10mg tds/prn Fentanyl Skin patch patch 25-50mcg/h Controlled over 72h drug Common drugs used in the department are in bold. Please consult if in doubt. Antiepileptics Phenytoin Indication Management of generalised tonic-clonic and complex partial seizures. Prevention of seizures post head trauma or surgery. Dosage Loading dose IV or PO = 15-20mg / kg; Give PO 300mg x 3 every 3-4 hrs or IV 1g over 30mins(NOTE: maximum rate of IV administration is 50mg/min) Maintenance dose IV or PO = 4-7mg / kg / day (Usual starting dose 5mg/kg/day) Therapeutic Drug Monitoring Check baseline LFT, preferably prior to starting the phenytoin. Phenytoin levels should be checked within 24 hrs post initiation, to ensure an adequate loading dose, as severe traumatic brain injury patients are at the highest risk of seizure in the early post-traumatic phase i.e. first 7 days. If levels are in the therapeutic range, re-check phenytoin and albumin levels 7-10 days post initiation. Therapeutic level = 10-20 mg/L Need to correct phenytoin with low albumin level:
Corrected Phenytoin level = 1___________ X Observed [0.2 x alb (g/L) / 10] + 0.1 Phenytoin level

There may be more free phenytoin in the serum, in end-stage renal disease patients. Where the levels are subtherapeutic, a mini-load may be used to ensure a more rapid achievement of therapeutic level, in addition to an increase in the maintenance dose: Mini-load (mg) = (15 corrected phenytoin level) x 0.7 x Wt (kg) Valproic acid may cause an initial decrease in serum phenytoin concentration. However, with continued combination therapy (approximately 3 months), monitor for increased toxic effects of phenytoin. There may be a decrease in valproic acid level due to the inducing liver enzyme effects of phenytoin. Duration of treatment It was demonstrated that the routine use of phenytoin, valproic acid, carbamazepine in the first week following TBI decreases the incidence of early-onset i.e. within 7 days of injury seizures but does not change the incidence of late-onset seizures. Check with Neurosurgeon if in doubt Adverse Drug Reactions IV: hypotension, bradycardia, cardiac arrythmia, cardiovascular collapse (especially with rapid IV use), thrombophlebitis. Concentration-related effects: slurred speech, dizziness, drowsiness, lethargy, fever, rash, nausea, vomiting, confusion nystagmus, blurred vision, diplopia, ataxia, Others: toxic hepatitis, liver damage

PHYSICIAN PROTOCOL FOR RUNNING IV PHENYTOIN VIA SYRINGE PUMP - Neuroscience ICU and Neurosurgery ICA
ALL loading doses of IV Phenytoin must be infused via a syringe pump. Equipment and Drug needed: Syringe Pump 1 X 10ml / 20ml / 50ml Syringe (depending on the Phenytoin dose) 1 X 20ml Syringe 5ml Normal Saline Phenytoin Injection 250mg per 5ml vial(s) Procedure: 1. Ascertain what loading dose (15-20mg/kg) of IV Phenytoin is needed, and calculate the actual dose to be given to the patient.
2.

Doctor to draw out the dose required (250mg/5ml vial) of neat Phenytoin Run the Phenytoin infusion at no faster than 50mg (1ml) per minute e.g.

Injection solution into a 50ml syringe and attach to the syringe pump.
3.

1g dose to run over > 20min. 4. Do not infuse together with any other drug and/or infusion solution in the same IV line. If concurrent infusion is absolutely needed, please check with the pharmacist first. 5. Prepare 5ml of normal saline in a 20ml syringe. 6. At the end of the IV Phenytoin infusion, remove the syringe.
7.

Flush the IV line by attaching the 20ml normal saline syringe to the pump.

Run 5ml of the normal saline through the line, at < 1ml per minute. This should take at least 5 mins.
8.

Please note that the doctor has to start the pump running and remain with

the patient in the ICU or ICA until the infusion is completed, to monitor for adverse effects e.g. hypotension, bradycardia, cardiac arrhythmias, cardiovascular collapse, venous irritation and pain, and/or thrombophlebitis. There should be continuous ECG and BP monitoring throughout the administration of IV Phenytoin.

Levetiracetam (Keppra)
Use Adjunctive therapy in the treatment of partial onset, myoclonic, and/or primary generalized tonicclonic seizures Pregnancy Risk Factor C Lactation Enters breast milk/not recommended Contraindications Hypersensitivity to levetiracetam or any component of the formulation Warnings/Precautions Concerns related to adverse effects: CNS effects: Weakness, dizziness, and somnolence occur mostly during the first month of therapy. Hematologic effects: Although rare, decreases in red blood cell counts, hemoglobin, hematocrit, white blood cell counts and neutrophils have been observed. Psychotic symptoms: Psychosis, hallucinations and behavioral symptoms (including aggression, anger, anxiety, depersonalization, depression, personality disorder) may occur; dose reduction may be required. Suicidal ideation: Pooled analysis of trials involving various antiepileptics (regardless of indication) showed an increased risk of suicidal thoughts/behavior (incidence rate: 0.43% treated patients compared to 0.24% of patients receiving placebo); risk observed as early as 1 week after initiation and continued through duration of trials (most trials 24 weeks). Monitor all patients for notable changes in behavior that might indicate suicidal thoughts or depression; notify healthcare provider immediately if symptoms occur. Disease-related concerns: Renal impairment: Use caution with renal impairment; dosage adjustment may be necessary. Concurrent drug therapy issues: Sedatives: Effects with other sedative drugs or ethanol may be potentiated. Special populations: Pediatrics: Safety and efficacy have not been established in children <4 years of age (oral formulation) or <16 years (I.V. formulation and extended release tablets). Children may have increased incidence of psychotic symptoms; dose reduction may be required. Other warnings/precautions: Withdrawal: Anticonvulsants should not be discontinued abruptly because of the possibility of increasing seizure frequency; therapy should be withdrawn gradually to minimize the potential of increased seizure frequency, unless safety concerns require a more rapid withdrawal.

Adverse Reactions >10%: Central nervous system: Behavioral symptoms (agitation, aggression, anger, anxiety, apathy, depersonalization, depression, emotional lability, hostility, hyperkinesias, irritability, nervousness, neurosis and personality disorder: adults 5% to 13%; children 5% to 38%), somnolence (8% to 23%), headache (14%), hostility (2% to 12%) Gastrointestinal: Vomiting (15%), anorexia (3% to 13%) Neuromuscular & skeletal: Weakness (9% to 15%) Respiratory: Pharyngitis (6% to 14%), rhinitis (4% to 13%), cough (2% to 11%) Miscellaneous: Accidental injury (17%), infection (2% to 13%) 1% to 10%: Cardiovascular: Facial edema (2%) Central nervous system: Fatigue (10%), nervousness (4% to 10%), dizziness (5% to 9%), personality disorder (8%), pain (6% to 7%), agitation (6%), irritability (6% to 7%), emotional lability (2% to 6%), mood swings (5%), depression (3% to 5%), vertigo (3% to 5%), ataxia (3%), amnesia (2%), anxiety (2%), confusion (2%) Dermatologic: Bruising (4%), pruritus (2%), rash (2%), skin discoloration (2%) Endocrine & metabolic: Dehydration (2%) Gastrointestinal: Diarrhea (8%), nausea (5%), gastroenteritis (4%), constipation (3%) Genitourinary: Urine abnormality (2%) Hematologic: Leukocytes decreased (2% to 3%) Neuromuscular & skeletal: Neck pain (2% to 8%), paresthesia (2%), reflexes increased (2%) Ocular: Conjunctivitis (3%), diplopia (2%), amblyopia (2%) Otic: Ear pain (2%) Renal: Albuminuria (4%) Respiratory: Influenza (5%), asthma (2%), sinusitis (2%) Miscellaneous: Flu-like syndrome (3% to 8%), viral infection (2%) <1%, postmarketing and/or case reports: Alopecia, anemia, catatonia, hematocrit decreased, hemoglobin decreased, hepatic failure, hepatitis, leukopenia, LFTs abnormal, neutropenia, pancreatitis, pancytopenia (with bone marrow suppression), psychotic symptoms, red blood cells decreased, suicide attempt, suicide behavior, suicide ideation, thrombocytopenia, weight loss Reconstitution Injection solution: Must dilute dose in 100 mL of NS, LR, or D5W. Mechanism of Action

However, several studies have suggested the mechanism may involve one or more of the following central pharmacologic effects: inhibition of voltage-dependent N-type calcium channels; facilitation of GABA-ergic inhibitory transmission through displacement of negative modulators; reduction of delayed rectifier potassium current; and/or binding to synaptic proteins which modulate neurotransmitter release. Pharmacodynamics/Kinetics Absorption: Oral: Rapid and almost complete Distribution: Vd: Similar to total body water Protein binding: <10% Metabolism: Not extensive; primarily by enzymatic hydrolysis; forms metabolites (inactive) Bioavailability: 100% Half-life elimination: ~6-8 hours; extended release tablet: ~7 hours; half-life increased in renal dysfunction Time to peak, plasma: Oral: Immediate release: ~1 hour; Extended release: ~4 hours Excretion: Urine (66% as unchanged drug) Dosing: Pediatric Myoclonic seizures: Oral: Children 12 years: Immediate release: Initial: 500 mg twice daily; may increase every 2 weeks by 500 mg/dose to the recommended dose of 1500 mg twice daily. Efficacy of doses >3000 mg/day has not been established. Partial onset seizures: Oral: Children 4-15 years: Partial onset seizures: Immediate release: 10 mg/kg/dose given twice daily; may increase every 2 weeks by 10 mg/kg/dose to a maximum of 30 mg/kg/dose twice daily Children 16 years: Refer to adult dosing. Tonic-clonic seizures: Oral: Children 6-15 years: Immediate release: Initial: 10 mg/kg dose given twice daily; may increase every 2 weeks by 10 mg/kg/dose to the recommended dose of 30 mg/kg twice daily. Efficacy of doses >60 mg/kg/day has not been established. Children 16 years: Refer to adult dosing. Dosing: Adult Myoclonic seizures: Oral: Immediate release: Initial: 500 mg twice daily; may increase every 2 weeks by 500 mg/dose to the recommended dose of 1500 mg twice daily. Efficacy of doses >3000 mg/day has not been established. Partial onset seizures: Oral: Immediate release: Initial: 500 mg twice daily; may increase every 2 weeks by 500 mg/dose to a maximum of 1500 mg twice daily. Doses >3000 mg/day have been used in trials; however, there is no evidence of increased benefit.

Extended release: Initial: 1000 mg once daily; may increase every 2 weeks by 1000 mg/day to a maximum of 3000 mg once daily. I.V.: Initial: 500 mg twice daily; may increase every 2 weeks by 500 mg/dose to a maximum of 1500 mg twice daily. Doses >3000 mg/day have been used in trials; however, there is no evidence of increased benefit. Note: When switching from oral to I.V. formulations, the total daily dose should be the same. Tonic-clonic seizures: Oral: Immediate release: Initial: 500 mg twice daily; may increase every 2 weeks by 500 mg/dose to the recommended dose of 1500 mg twice daily. Efficacy of doses >3000 mg/day has not been established. Loading dose (unlabeled): Immediate release: Initial doses of 1500-2000 mg have been welltolerated (Betts, 2000; Koubeissi, 2008), although the necessity of a loading dose has not been established Dosing: Hepatic Impairment No adjustment required End-stage renal disease patients using dialysis: 500-1000 mg every 24 hours; a supplemental dose of 250-500 mg following dialysis is recommended Administration: I.V. Infuse over 15 minutes

Valproic Acid (Sodium Valproate) Indication Management of generalised tonic-clonic and complex partial seizures. Prevention of seizures post head trauma or surgery. Dosage Initiate at 10-15mg/kg/day IV or PO in 1-3 divided doses. Increase by 5-10mg/kg/day at weekly intervals until therapeutic levels are achieved. Usual adult dose: 1000 to 2500 mg/ day ; Administer IV dose at < 20mg / min. Single doses up to 15mg/kg have been administered as a rapid infusion over 5-10min (1.5 3mg /kg/min). The controlled release preparation (Epilim Chrono ) should be administered om/bd Therapeutic Drug Monitoring Check baseline liver function tests, preferably prior to starting the valproic acid. Levels should be checked 4 days post initiation to ensure adequate dose. Therapeutic level = 50-100 mg/L Drug-interaction with phenytoin Duration of treatment As for Phenytoin; see entry as for phenytoin. Adverse Drug Reactions Somnolence, dizziness, insomnia, nervousness, nausea, diarrhea, thrombocytopenia, increased AST & ALT, blurred vision, myalgia. Strengths, dosage forms & cost
Valproic Acid Injection 400mg/4ml = $52.70 (standard drug, list 2)

Sodium Valproate 200mg = $0.20 (standard drug) Valproic Acid Chrono tablet 500mg (Epilim Chrono) = $0.80 (standard drug) Valproic Acid Suspension 200mg/5ml = $8.20 per 100ml (standard drug)

Carbamazepine Indication Management of generalised tonic-clonic and complex partial seizures. Prevention of seizures post head trauma or surgery. Dosage Usual dose: 200mg bd to tid If patient was on phenytoin before, initiate at 200mg tid. May increase by up to 100mg / day until therapeutic levels are achieved. Therapeutic Drug Monitoring Check baseline liver function tests, preferably prior to starting the carbamazepine. Carbamazepine levels should be checked 4-7 days post initiation and after any dose change to ensure adequate dose. Therapeutic level = 4-10 mg/L Duration of treatment See entry as for phenytoin. Adverse Drug Reactions Arrythmias, hypo-/hypotension, dizziness, sedation, comnolence, nausea, vomiting, diarrhea, abnormal liver function tests, thrombocytopenia, leukopenia. Strengths, dosage forms & cost
Carbamazepine 200mg = $0.10 (standard drug) Carbamazepine CR 200mg (Tegretol) = $0.15 (standard drug); CR 400mg (Tegretol) = $0.45 (standard drug)

Common Neurosurgery drugs Labetalol Class Beta-blocker Indication Hypertensive emergencies Dosage IV Usual dose: 5 20mg / hour Consider starting an oral beta-blocker e.g. atenolol once patient is more stable. Duration of treatment Until hypertensive emergency resolved. Adverse Drug Reactions Bradycardia, hypotension, dizziness Strengths, dosage forms & cost Labetalol injection 25mg/5ml = $6.80 (non-standard drug) Mannitol Class Osmotic Diuretic Indication Reduction of increased intracranial pressure (ICP)

Dosage 0.25 to 1g / kg over 15 to 30 mins, every 4 to 6 hours. This is equivalent to 75 to 300ml of Mannitol 20% every 4-6 hours for a 60kg patient. Keep serum osmolality < 320mOsm to decrease risk of renal failure and maintain euvolemia by adequate fluid replacement. Rebound increase in ICP may occur. Mannitol is contraindicated in patients with chronic, severe renal failure or those renal failure patients unresponsive to a test dose. Duration of treatment Dependent on Neurosurgeon. Adverse Drug Reactions Fluid and electrolyte imbalance: dehydration and hypovolemia, hyponatremia, congestive heart failure, pulmonary edema, hypotension, increase in cerebrospinal fluid osmolarity (thus worsen or impair the lowering of intracranial pressure), hyperkalemia, acute renal failure. Strengths, dosage forms & cost Mannitol Infusion Solution 20% 250ml (20g/100ml) = $4.00 (standard drug)

Nimodipine(Nimotop) Class Calcium Channel Blocker Indication Prophylaxis and treatment of ischaemic neurological deficits caused by cerebral vasospasm following subarachnoid haemorrhage (SAH). To commence within 96 hours of the SAH. Dosage Intravenous: 1-2mg/hour (given neat) Oral: 60mg every 4 hours Duration of treatment : 21 days This is because after an SAH, both vasospasm and delayed cerebral ischemia typically begin at day 3, peak between days 7 and 12, and may continue through day 21. Adverse Drug Reactions Marked decrease in blood pressure, headache, flush, sweating, dizziness, gastrointestinal complaints (nausea, diarrhoea, abdominal cramps), reduction in heart rate. Strengths, dosage forms & cost Nimodipine Infusion solution 10mg /50ml = $84 (non-standard drug) Nimodipine tablet 30mg = $2.60 (non-standard drug)

Vancomycin Class Antibiotic Indication MRSA or methicillin-resistant Coagulase Negative Staphalococcus Infections Please follow our SGH vancomycin guidelines on use. Dosage Usual dose: 10-15mg/kg bd Patients with renal impairment may require less frequent dosing e.g. 24 hours or more. Usually infused over 1 hour. With higher dosages or patients who experience the red man syndrome, the drug may be infused over 2 hours. Therapeutic Drug Monitoring Check a vancomycin trough level at the 4th dose. In renal failure patients with intermittent dosing, please ask your pharmacists for help with regards to checking levels. Therapeutic level = 10-15 mg/L (higher levels may be warranted for severe infections, please consult your ID physician or pharmacist). Adverse Drug Reactions
Red man syndrome if infused too rapidly, drug fever, chills, thrombocytopenia, neutropenia Vancomycin Injection 500mg = $3.05 (standard drug, list 2)

Strengths, dosage forms & cost

Glossary

Cardio AMI Ix: 4tubes, CK, CKMB, Trop T+Bedside TropT, +/- LFT, +/- ABG. CXR, ECG: ST elevation +/- Q waves. R sided leads if ?Inf AMI. NB: Trop T increased in CRF, recent AMI. CKMB/CK ratio > 5%. Rx: O2. CRIB. Aspirin 300mg x1, then 100mg om [CI: BGIT, anemia ?cause], else Ticlid 250mg om. GTN / S/L or patch stat.[CI: low BP] ISDN 10mg tds. Atenolol 100mg om [CI:asthma]. Captopril 12.5mg bd if ant AMI. Major MI: add Morphine 5mg i/v + maxalon.

Atenolol 5mg i/v over 5 min. ISDN 2-10mg/h i/v. Urgent cardio r/v if good premorb & major MI. CCF Ix: 2tubes, CEnz, LFT, +/-ABG, ECG, CXR Rx: Fluid restrict 1L/day. i/n O2, I/O chart, RIB iv Lasix 40-80mg x1 + 40mg bd, spanK 0.6g om Chest pain (on call) Read case notes: PMH, current dx, recent ECG/CE. Hx/PE: Nature of pain: cardiac/pleuritic/m usculoskeletal Ix: ECG(ST elevation, Q waves, then T inversion), cardiac enz.

Collapse/CPR Determine status over phone. See stat anyway. A,B : 100% O2 Bag, Dentures, Oral airway.Synchroniz e if breathing. C: No pulse = pump 5:1. i/v access + 5mls bld & h/c. i/v N/S 1 fast. - Asytole: 1mg adrenaline (1 adrenaline) + 1 mg atropine x 3 - VT/VF: off GTN, defib pads, align apex. Clear. 200J, check rhythm, 360, check, 360 then adrenaline 1mg, lignocaine 70mg - PEA/EMD: Tx as for K+ . Excl pneumothorax,

cardiac tamponade. If still no response & no help: Check premorbid, case sheet. - Intubate: Preoxy. Wear mask. ETT: Males: Size 8 to 22-24cm. Fem: Size 7.5 to 2022cm. Visualize, intubate, check both lungs, SaO2. - I/v HCO3 50mls after 5 mins. DIM Alcohol intoxication Ix: 3 tubes, alc toxi (document no alcohol swab), +/green tube. Rx: Valium 2mg, 2mg, 5mg for Delirium tremors. Folate 10mg om, Vit B Co / bd, Thiamine 30mg om

Cellulitis Ix: 2 tubes, Bld C/S, wound swab. Hba1c(DM)/Fastin g h/c 4 tubes, ref ortho for abscess, OM, necrotizing fasc, wet gangrene. Rx: (1)i/v Clox 1g 6h, (2)i/v ampi 1g 6h or CP 2mU 6h. Paracet. Hypotension (while on call) Order 1 N/S(no K+) fast over phone. Confirm BP. Dx type of shock. Ix: 4 tubes, +/- CK, CKMB, ECG, +/DIVC screen, +/lactate Rx: O2, Fluids fast (> 2L unless in CCF). Call MO if still poor response. Kiv dopamin 110g/kg/min. kiv CVP. Kiv PCT. Poisoning Ix: 4 tubes, LFT, toxicology (green tube, urine, sign 4 seals and fill form). ABG(Salicylates), levels(paracet/sali cylate/etc) police case, refer MSW, suicide precau Rx: Lavage [<2h], charcoal. 50g 4h [<4h] Paracet=n-ac (abv). Off later if 4h>200mg/L (1.3mM), 12h>50mg/L

Salicylate. If lvls > 3.6mM, give 1.26% bicarb +/hemodi. Cx=Fits(diazepam ), Acidosis(bicarb) Naloxone 2mg/2min max 10min then 2mg in 1/titrate rate Theophylline: Tx hypokalemia, diazepam for fits, Potassium -Low: Ix: +/ECG(Inverted T,U wave, PR , ST ), repeat K+ 6h/cm Rx: <2.5 or < 3.0 with digoxin tox/AMI/IHD for op: potassium 7.45% 10mls in 100ml N/S i/v over 1hr max 20mmol/h, (max 20mmol/, do not flush) Stop diuretics or add span K. Treat cause (eg vomitting) High: Ix: ECG(Tall T,wide QRS, small P), repeat K+ in 6h/cm More leeway(add 0.5) in: ESRF, recent AMI, lysed > 5.0: Resonium 15g stat/30g fleet & 15g 8h po > 5.5: add glucose 50% 40mls(dilute w/ N/S) + insulin 6U i/v > 6.0: Calcium gluconate 10% 20mls slow i/v (cardioprotect), +/- neb ventolin: N/S 1:3 stat. ECG, Cardiac

monitoring. +/Hemodialysis. Stop K+ sparing diuretics, treat ARF(eg hydration) Sodium Low (<125): True Na+ = Na+ + gluc/4 (esp in DKA) Dry: 0.9% N/S [(125Na+)*0.6*wt 154 ] litres /24h - 125=target Na(max by 10/24h). 514(vs 154) for 3% N/S. stop diuretics. Euvolemic: SIADH(malig,CNS, chest,metab,drugs ),iatrog Ix: CXR, fT4, TSH, LFT, cortisol. Plasma osm. Urine osm, Na+. 8am: cortisol, reninangiotensin ratio(2 FBC tubes), U/E.- Fluid restrict 1L/d +/- Saline +/Lasix . Stop D5% drip. Overloaded: CCF, CRF, hypoalb. Diuretics. High: Encourage plain water intake else D5% drip 35L/24h. Large amt urine: ? DI. Low K+, high bicard: ? Aldosteronism. Endocrine Newly Dx DM Ix: 2 tubes, LFT, HbA1c, Fasting lipids, fT4/Tsh ECG,CXR, Later: microalb kiv

24CCT & UTP. Dietician, DNE, Fundal photo Rx: DM 15001800kcl, tds+10, SCSI accordingly DKA/HHNK (H/C HI, Acidotic, patient sick/drowsy) Ix: 2 tubes, ABG, CXR, Urine ketones(stat dipstick). +/- 4 hour U/E/ABG (consider HD/ICU). +/- Cenz, ECG. Rx: NBM, hourly(you do)-2 hourly h/c, hourly parm. I/O +/catheterize. +/CLC if drowsy. I/v actrapid(SI) 6U stat then infusion: 50U SI in 49.5ml N/S(1U/ml) at 6mls/hr then change N/S above to D5% at 3mls/hr once BSL<12. i/v N/S 2L/2h + add K+ 20-40/hr if pu. Overlap SCSI with i/v insulin for 1-2h when converting iv to SCSI. Hyperglycemia (while on call) 1)(a)8-12, (b)1216 with DM meds due, (c)12-16 at 10pm: Watch. 2)12-16, no SCSI/oral meds due: SCSI 6-8U 3)16-20: SCSI 810U. 4)20-24: SCSI 1012U. Recheck 24hrs, kiv urine ketones.

5)>24: Consider DKA workup. Consider adjusting pts oral meds (esp outside of Medical). Hypoglycemia (while on call) H/C: <2.5: I/v D50% 20-40mls (dilute with N/S). add i/v thiamine 100mg if alcoholic. <3.0: Glucose drink. Recheck hc 2-4h later. Then: i/v D5 or D10% drip esp if NBM. Off OHGAs & insulin. If admitted for workup: Write meds in casesheet. Any OD? Diet hx. Stop DM meds. Ix: 2 tubes, HbA1c, excl infection. H/c 2-4 hrly. Synacthen test Ix: i/v 250g synacthen (send IMR early in morning).Cortisol at 0, 30 and 60 min (can site plug in elbow). Any > 500 = responsive. Gastro Abdominal pan (while on call) Causes: GI, HBSPanc, KUB.Cardio, lung, AAA. DKA, Ca+, psych. PE: +/- PR. Exclude acute abd. Ix: 4tubes, LFT, amylase, Ca+, Po4. AXR/erect

CXR, +/- cardiac enz & ECG. +/Ufeme, C/S. Urine pregnacny. Rx: NBM, PFO if surgical abdo. Else MMT/Mist carb/famot. BGIT On iron tabs? PR Ix: 4tubes, LFT, Cenz, stool OB if no obvious bleed. anemia workup (2 plain + 1 fbc) before transufsion. +/- ECG. AXR if ? perf. Rx: NBM, i/v drip, Off NSAIDS. i/v pantoprozole 40mg bd then omeprazole 40mg bd/om po after scope add i/v somatostatin if suspect varices (liver cirrhosis, alcoholic) GE Ix: 2tubes, LFT. AXR if?IO. Stool C/S, ova-parasites. +/- bld c/s, +/Stool for leucocytes and Cdifficile. NBM>Clear feeds>Non-milk diet. Rx: i/v 2-3 N/S + 2D5%/24h. stat doses of i/v N/S if dry. I/v maxalon 10mg tds/prn.Kaolin 10mls tds if severe diarrh. Ciprofloxacin if septic. Hepatitis

Ix: 3tubes,LFT. Acute Hep Sero, ? CMV, EBV. LFT/PT,PTT eod. Rx: Vit B / om. Low fat diet. Stop hepatotoxic drugs. Hepatic encephalopathy Ix: 4tubes, Ca/Mg/P, ABG, Bld C/S. FP. Rx:i/v multivit 10mg, i/v thiamine 100mg, i/v vit k 10mg x 2/7. Lactulose. Folic acid, vit b co, sangobion. Propranolol. Low protein diet. Heme-Onco Anemia Hx: Diet, Gastritis, NSAIDs, Menorrhagia PE: PR, Postural BP Ix: 4 tubes, LFT, ECG, Fe,TIBC/Ferritin(Pl ain tube), B12,Folate(Plain tube, FBC form), PBF, Retic.(FBC tube) +/- Hb Electrophoresis, +/- Stool OB x 3/7. kiv OGD. Rx: RIB, O2.1 PCT/4 hours (after workup up) if Hb < 10. Lasix 20mg with PCT if overloaded/phx IHD. Blood reaction Ix: Fill form. GXM tube, Grey tube. Hourly parm, +/O2.

Rx: Hydrocort, Piriton. Blood transfusion/call BTS MO (on call) Know: Hb, blood group, Dx, symptomatic/blee ding? pre-op? Document reply. Check blood: Num on tag vs packet. Name on tag vs pt. Sign. Lasix? DIVC screen (PT/PPT tube & form) Ix: Fibrinogen( ), D-dimer >0.5, soluble fibrin monomer DVT Ix: Leg circumference. ddimer, Anticardio lipin Ab. Duplex scan. Rx: S/C clexane 1mg(0.1ml)/kg bd Neutropenic sepsis Ix: 3tubes, LFT, Bld C/S, ECG, CXR, Ufeme & C/S Rx: i/v cetriaxone 1g om + i/v genta 80mg tds OR i/v fortum 2g bd + i/v amikacin 7.5mg/kg bd if nosocomial PT/PTT raised (pre-op) No i/m injections, fall precautions, RIB. Ix: LFT, +/- DIVC screen (see above). Recheck pt/ptt <when>.

Rx: i/v vit k 10mg om x 3/7 for raised PT. 500mls FFP 8 hourly if for invasive procedure. Inform surgeon. Not for spinal/epidural. ID Dengue PE: Bleeding, Postural BP Ix: 4tubes, LFT, Dengue Sero, BFMP, +/- Bld C/S Ufeme, Stool OB, Daily FBC, CRIB, Notify. No i/m inj (if plt low) Rx: Paracet Malaria PE: Cerebral, pulmonary cx, Postural bp (hypovol) Ix: FBC (Hb < 8), PBF (for schizonts), BFMP. LFT (Cr > 205, Bil > 50). PT/PTT kiv DIVC screen. Bld C/S. G6PD level(FBC tube). Kiv Dengue, wwF. +/- BFMP x2 12 hourly (finger prick & smear) H/c 6h (hypoglyc). Rx: Chloroquine 600mg stat and 300mg om x 3/7 If toxic, above criteria +ve, or BFMP falciparum: Quinine: Load (wt x20) in 1 D5% i/v over 4h then (wt x 10) in D5 over 4-8h bd-tds Sepsis Guidelines:

Cellulitis: Cloxacillin 0.5-1g 6h + CP 2mu 6h/Ampicillin 500mg 6h GE, severe: >6x, fever, toxic: Ciproflox 500mg bd po/400mg bd i/v Meningitis: ceftriaxone 2g bd i/v after bld c/s but before LP Neutropenic sepsis: (1)Ceftriaxone 1g om + Gentamycin 120mg om Or (2)Imipenem 0.5g 6h i/v or cefepime 2g om or Fortum 2g bd i/v + amikacin 7.5mg/kg bd i/v or . Regime varies by dept/hsptl. Peritonitis - SBP: ceftriaxone 2g om i/v Peritonitis - perf: Ciproflox 400mg i/v 12h + Flagyl 500mg i/v 6h Pneumonia, mild: Amoyxcillin/Augm entin po + EES. Alt: Clarithro. Pneumonia, CAP: ceftriaxone 1g om i/v + EES 800mg bd po Pneumonia, CAP, severe: above + cloxacillin 1g 6h i/v Pneumonia, nosocomial: imipenem 500mg 6h or pip-tazo 4.5g 6h Pneumonia, aspiration: ceftriaxone +

metronidazole 500mg 8h i/v Septic arthritis: tap, i/v ceftriaxone 1-2g qds + ? cloxacillin 1g 6h Septic shock: imipenem 0.5mg 6h i/v or meropenem 1g 8h Thrombophlebiti s: cloxacilln 500mg 6h x 2/7, GMS dressing UTI: urine dipslide, i/v ceftriaxone1g om, or po ciprofloxacin 250mg bd or po bactrim / bd or po augmentin 525mg bd Neuro Bells palsy (usu not admitted unless to excl stroke) Ix: EBV, HSV, CMV, ESR. Blink reflex. Rx: Pred 40mg om x 2/7 -> 20mg om x 5/7. Eyedrop/shield. CVA Ix: +/- CLC 4 hourly. NBM/NG feeds if dysphagia. PT/OT/ST. 3 tubes, LFT, Ca/P. ESR, VDRL, fasting lipids & glucose. ECG, CXR U/S carotids, CT head (usu already done, non-contrast) Rx: Aspirin 100mg om + famotidine 20mg om-bd, after excl. CI. BP up to 160/100 normal post-CVA: dont treat.

Drowsy/Confusio n Causes: Structural, infective, metabolic, drugs, any organ failure Ix: h/c stat. +/CLC. Off sedatives. Ix as for provisional dx: Struc: CT head + CVA workup. Infective: septic workup +/- LP. Metab/drugs: 4 tubes, SpO2, ABG, toxi. Epilepsy/Fits Ix: h/c stat. 100% O2. I/v plug 2 tubes, antiepileptic levels (send all if unsure), LFT, CK, CKMB, aldolase. Later: ABG, bld C/S. CT head. Rx(Pt fitting):Diazepam 5mg slow bolus max 15mg. 2nd line: phenytoin 20mg/kg (undiluted, or in a line running N/S) with BP and cardiac monitor. If h/c < 4: i/v D50% 40mls (with thiamine 100mg i/v if ?alcoholic) Maint: Phenytoin 300mg 6h x 3 then 300mg om Giddiness, postural hypotension Causes: CNS, Vestibular, Cardiac, Metab/drugs

PE: Nystagmus, cerebellar s/s, postural BP, Hallpikes, gait Ix: 4 tubes, Cenz, h/c, ECG, Rx: Stugeron / tds/prn, Stemetil 10mg tds/prn LP/Meningitis Ix: Consent, CT head, h/c, Plt & PT/PTT. Opening P. Fluid for: (1clearest)Feme(tw/ gluc), (2)G Stain and C/S, (3)AFB and TB C/S, (4)Fungal smear and C/S. kiv for (5)Latex agglutination, (6)Neurotrophic viruses, (7)VDRL, (8)Cytology Rx: i/v ceftriaxone 2g stat & bd after bld c/s, before LP/CT. Renal Diet Pre-HD: Cr < 300: Prot 1g/kg/d. >400: 0.60.8g/kg/d HD: Prot 0.81g/kg/d, low K, Na+,fluid 500+urine CAPD: Normal Prot(60-80g), K. Na and fluid restrict. Dialysis pt Hx: Dialysis days/center. Last HepB/HIV. Fluid restriction. Ix: 3tubes, ABG, ECG, CXR. Inform Renal MO cm. No

BP/blood taking L/R arm. Rx: Fluid restrict. DM/low salt diet. O2. i/v lasix 120240mg if overloaded and still having PU. Urgent HD if SOB+ +/K+ high. Nephrotic syndrome Ix: 3 tubes, Hep B,C, ANA, dsDNA, ANCA, RF, F Lipids. Ufeme, C/S, 24UTP, CCT. ECG. CXR, XR T/L spine. IO chart, daily wt. U/S kidneys. Rx: Fluid restrict 500. i/v lasix 80mg tds + span K. Dont start pred. Pyelonephritis Ix: 3tubes, Bld C/S, Ufeme + C/S. Genta levels Rx:Cefzolin 1g 6h + Genta OR i/vCiprofloxacin 250mg 12h OR Renal impair: Ceftriaxone 1g stat+om UTI Ix: 4tubes, Bld C/S, Ufeme & dipslide before ab Rx: ceftriaxone x 5/7/ Bactrim(nephrotox )/ Cipro/Augmentin Catheter assoc + S/S: kiv trial off catheter, ab x 14/7. Respiratory

Asthma(Reversi bility)/COPD Ix: 2tubes, ABG(on x l/min), ECG, CXR, Peak Flow. (asthma) Rx: i/n O2 2L/min, +/- rib. Off blockers. Neb ventolin:N/S 1:3(asthma) or ventoline:atrovent :n/s 1:1:2(COPD) 2-6 hourly, i/v hydrocort 100mg 6h or pred 1030mg x 3/7. Rx any pneumonia. Hemoptysis Ix: 4tubes, LFT, hemoptysis chart(>25 x1 or >300/24h). Sputum C/S. +/cytology. +/-TB ix. +/- blood C/S if ? pneumonia. CXR(Bronchiec). Kiv E-bronch Rx: procordin 10mls tds. If massive(die from asphyxia, not blood loss): Lie on affected side(see CXR). 100% o2. Suction. Intubate (kiv w/ 2 lumen ETT). E-bronch.. kiv pulmonary art. embolization. PE Ix: 4 tubes, ABG + A-a gradient. Spiral CT. V/Q scan if spiral CT contraindic. Duplex LL. Rx: 100% O2, Clexane bd Pleural tap

Consent. Ix: Serum: LDH, LFT, +/- tumour markers Fluid: 1 + ABG tube: Feme, protein, LDH, pH 2:G stain and C/S. 3: Cytology. 4:AFB, TB C/S 5:Fungal 6:Cryptococal Ag Lights: Any of: Pl/serum: TP>0.5, LDH>0.6. Pl abs: LDH>200. Pneumonia Ix: 3tubes, ABG, Bld C/S, +/mycopl/leg/chlamy dia sero Ufeme + C/S, Sputum stain + C/S, AFB smear + C/S kiv laryngeal swab for AFB & TB C/S x 2/7, mantoux Rx: i/n O2 2L/min. Chest physio Ceftriaxone 1g stat+om, EES 800mg bd/tds, paracet Hsptl acq: cefepime/pip-taxo (Pseudomonas) Aspiration: Metronidazole Allergy to penicillins: EES/Doxycyclin/Cl arithromycin Pneumothorax Ix: 4 tubes(2 if small), SpO2/ABG, CXR (in full inspiration), ECG Rx: 100% O2(even if not SOB) -> Chest tap -> Chest tube (4

tubes, consent, repeat CXR post tube). Shortness of breath (on call) Get dx , increase O2 over phone except COPD. Read casesheet. Ix: 3tubes, SaO2/ABG, +/Cenz & ECG, CXR. +/- PE ix. Rx: O2 (keep < 4L/min if known Type 2 RF), tx cause Pre/Post op / procedure Pre-op prep. PFO Prepare for op All: Listing, OT chit, consent. NBM 12mn(except under LA). Premeds on call to OT: Eg i/v cefazolin 2g <40, minor: Hb >40, minor: FBC, U/E, ECG, CXR major: FBC, U/E, CXR. if > 40, +ECG Rheumatoid Art going for GA: Cspine (Flex/Ext) Bronchoscopy: FBC, ECG. PT/PTT if for TBLB. I/m pethidine 30mg + i/m atropine 0.6mg(CI: Tachycardia, phx AMI) on call to ot OGD: NBM 12mn. Bowel Prep (colonoscopy): Low residue x 3/7, feeds only x 1/7, PEG 2L/Oral fleet 45ml bd x 1/7 before +/- Fleet

enema few hours before. Post-op review Read op findings, post-op instructions and copy. Check: VS stable. Dressing not soaked? (dont open!), drain unclamped, drain not excessive. Distal perfusion & neuro ok. Order: Hourly parm, O2, pain relief, 1st dose of stuff, Feeds>DOC, STO x POD. Interventional radiology (TACE, Angiogram, Hickmans, etc) PE: Femoral pulse Ix: Consent, 4 tubes, LFT, Cr , Hb>8, Plt > 100k, PT/PTT Pre: +/- nacetylcysteine 600mg bd Post-op: Examine wound site. RIB. Hourly parm, circulation chart x 6h. Pain relief. Tap/tubes/Cope loops Consider sedation and LA. Send for:1)Cytology 2)C/S, Gstain 3)TB C/S, AFB. 4)Biochem: FEME, TW, glucose, Pleural: 5)LDH, TP, SG, pH(ABg tube) 6) Serum h/c, LDH, TP.

LP: 5)Cryptococcus stain & Ag. 6)Specialized tests as ordered Joints: 5)Crystals Document: <Time>. <Procedure> and complications explained to pt. Performed by <Dr> under aseptic technique at <location>. Successful first attempt. <opening pressure>. 20mls of straw coloured fluid obtained and sent for <ix>. No cx, patient tolerated procedure well. Lie flat, hourly parm x 6 and CXR. <sign> GS Acute abd Ix: PR. 4 tubes, amylase, LFT, Ca+, Cenz. H/C. Urine diastase, pregnancy test. Ufeme, C/S. ECG, AXR, CXR(sitting/erect/L lat decub AXR). Hourly parm, NBM. Kiv CT abdopelvis. PFO. Rx: i/v fluids. Pain relief(strong relief only if confirm op). Ciproflox 400mg 12h i/v or Ceftriaxone 2g om, Metronidazole 500mg 8h i/v. ARU / BPH / Catheterization

Ix: PR, Ufeme, C/S, FBC, U/E/Cr, +/PSA +/- KUB Rx: Catheterize if pain/UTI/ARU. 12 small, 16 big. Replace foreskin. C/I: Pelvic #, prostatitis. In-out cath: Cath, measure amt, if < 300mls, remove cath. Suprapubic cath falls out: Use normal foleys, insert through track as per normal ASAP before track distorted. Call uro ASAP if cant cath. Cholecystitis/ biliary colic/ cholangitis. Ix: 4 tubes, amylase, LFT, Cenz, Bld C/S. Urine diastae. AXR(10% gallstones). U/S HBS. NBM. Rx: i/v fluids. Pain relief. Ciproflox 400mg 12h i/v or Ceftriaxone 2g om, Metronidazole 500mg 8h i/v. IO Ix: PR +/- flatus tube. 4 tubes, LFT, Cenz. H/C. ECG, AXR, CXR(sitting/erect/L lat decub AXR). Hourly parm, NBM. I/O chart. Kiv CT abdo. PFO esp if large bowel(haustra incomplt cross) >8cm , RIF tender, BS ++.

Rx: drip & suck(NG tube on intermittent suction). Fleet enema. Ciproflox 400mg 12h i/v or Ceftriaxone 2g om, Metronidazole 500mg 8h i/v. Testicular torsion D/dx: Epididymitis(>30y rs old usu), UTI, tumour, trauma, hydrocoele. Ix: 4 tubes. +/urgent doppler U/S. PFO. Consent for kiv orchidectomy & bilat orchidopexy. Rx: Pain relief, PFO. Ortho/Eye Eye emergencies Redness + Pain + decreased Va + = glaucoma/keratitis /iritis Blindness(sudden) + RAPD + white fundus & pale disc = CRAO Peripheral vision loss +/- curtain +/- floaters = retinal detachment Antibiotics/Anti microbials Amoyxcillin 500mg 8h po Ampicillin 500mg 6h i/v bolus Augmentin 625mg 12h po, 1.2g 8h i/v bolus/slow inf. Bactrim (Cotrimox) 2/2

(960mg) bd po [CI:CRF] Cefazolin 1g 8h i/v (2g on call to OT) bolus Cefepime 1-2g om-bd i/v [4th gen cephalosporin] Ceftazidime(Fortu m) 1g 8h/2g 12h i/v infusion [pseudmonas] Ceftriaxone 1-2g om i/v bolus(1g)/infuse(2 g), 2g bd[meningitis] Cefuroxime(Zinnat ) 500mg 12h po [2nd gen cephalosporin, po] Cephalexin 5001000mg 8h po Ciprofloxacin 500mg 12h po, 200-400mg 12h iv infusion Clarithromycin(Kla cid) 500mg bd po Cloxacillin 500/1000mg 6h i/v bolus/infusion 500mg 6h po Crystalline Penicillin 2mU 6h i/v infusion, [5mU per vial] Doxycycline 100mg bd po Erythromycin 500mg 6h po/iv, EES 800mg 12h po Gentamicin 4080mg(1mg/kg) 8h or120mg om i/v infus [chk lvls] Imipenem 500mg 6h i/v Metronidazole(Fla gyl) 400mg 8h po, 500mg 8h i/v infusion Penicillin V 500g 6h po

PiperacillinTazo(Tazocin) 2.25-4.5g 6-8h i/v [pseudomonas] Vancomycin 0.51g om-12h i/v [chk lvls] Others: Acyclovir 800mg 5x/d x 7/7, 500mg 8h i/v Chloroquine 600mg base(4/4) x1 then 300mg [chk G6PD] om po Quinine: Load (wt x20) in 1 pint D5% i/v over 4h then (wt x 10) in pint D5 over 4-8h bdtds [Falciparum malaria] TB: Mantoux(10U(0.1 ml) i/d)(occ. 1U). 10mm wheal = +ve Rifampicin 450mg(600mg if > 50kg) om po x 6/12 [liver] Isoniazide 300mg om po x 6/12[liver] + Pyridoxine 10mg om Pyrazinamide 1.5g om x 2/12 [liver] Ethambutol 600mg(15mg/kg) (=100mg) om x 2/12 [if 4th required] TripleRx(SGH): Clarithromycin 500mg bd po + Amoxycillin 1g bd po + Omeprazole 20mg bd po x 2/52 Allergy/Antiinflamm/Antihistamines/Ster oids

Dexamethasone 8mg 8h i/v, 0.510mg/d po Chlorpheniramine( Piriton) 4mg 6-8h po Hydroxyzine (Atarax) 1-25mg tds [itch] Loratidine (Clarityne) 10mg om po Fludrocortisone (Mineralocorticoid) 50-300mcg/d po Hydrocortisone 100-200mg 6h i/v, 20mg om+10mg on po Prednisolone 1030mg om po then 2.5-15mg/d maint Promethazine(Phe nergan) 25-50mg x1 po i/v i/m Synacthen test 250g x1 at 0 min, check 0, 30, 60. Asthma Aminophylline: Load 6mg/kg/20min i/v (not on theopylline) then 25mg/h. (25mg/ml in D5%, theophy lvl 10-20mg/L) Hydrocortisone 100mg 6h i/v Neb Ventolin:Atrovent: N/S 2: (0):2(asthma), 1:2:1 4-6h(cold) Prednisolone 30mg om po x 5/7 Theophylline(Neuli n) 125mg tds-qds po, SR 125mg bd po Relievers:Atrovent (20g)(Ipatropium MDI) 2/2 bd

Ventolin(Salbumat ol) 4/4 qds/prn MDI, 4mg tds/prn po Preventers: Becotide(50g) (Beclomethasone MDI) 2/2 bd-tds Flixotide(250g) (Fluticasone MDI) 1/1-2/2 bd Pulmicort(200g) (Budesonide turbohlaer) 2/2 bd Calcium: Calcium: [(40-Alb) x 0.02] + Ca+ Low: Ca gluconate 10% 10ml over 10min then 40mls/24h. Ca et vit D / om/bd po, Calcichew 6251250mg om/bd High: Calcium: [(40-Alb) x 0.02] + Ca+ (1)Stop thiazides. (2)N/S i/v 1L/hour or 4L/24h (3)Pamidronate (bisphosphonate) 60mg in 300ml N/S over 4 hour Cardio-Vascular Aspirin 100mg om po + famotidine 40mg bd Clexane 1mg/kg s/c om(prophy)bd(tx) [LMW Hep] Digoxin 62.5250mcg om po [lvls] Dopamine 25mcg/kg/min i/v[200mg in 0.1L NS at 2-7.5ml/h] GTN (0.3g) / s/l max x3. Patch(Nitrodisc) 510mg/24h

Heparin 1525U/kg/hr i/v infusion,see oporders, check PTT 6h ISDN 10-20mg bdqds po, SR 40mg bd.[angina,lvf] ISMN(Imdex 3060mg om)(Ismo 20mg bd-tds) po[angina,ccf] Ticlopidine(Ticlid) 250mg bd po Warfarin: Load 5,5,3mg om then check PT,INR. [counselling] AMI: Tall T,ST elev,Q wave,T inversion, TropT in non-CRF,O2. Aspirin 300mg chewed. Morphine 5mg i/v + maxalon.GTN / S/L or patch. Ace-I if Ant MI/LVF. +/anticoag.CPR: ABC, h/c, K+. Bag. No pulse=pump. Fluids fast/lasix. VF,VT:200,200,36 0. Asystole:Adrenalin e 1mg(10mls 1:10k) @ 5mins, Atropine 1mg max x3. Lignocaine 1mg/kg i/v. HCO3 40mls i/v after 10mins. Cholesterol/Lipi ds Gemfibrozil 0.30.6g bd (Triglycerides) Lovastatin 20mg on (LDL,total) (CI: liver dz) Simvastatin (Zocor) 10-40mg on (LDL,total)

Constipation Fybogel / om [bulk] Lactulose 10mls tds, 30mls in hep encephalopathy [osmotic] Senna / on [stimulant] Supp: Dulcolex/Fleet enema Bowel prep: Oral fleet 45ml bd, PEG 2L Cough Bromhexine (Bisolvon) 8mg or / tds (expectorant) Dequalium or Difflam lozenges / tds/prn (sore throat) MBE 10mls tds(black) (expectorant) Procordin 10mls tds(red) (suppressant,hem optysis) Creams, Dressings and Topical solutions Aqueous cream (dry skin) Calamine lotion (itchy skin) GMS dressing (plug site cellulitis) Wounds: Dry/Chlorhex/TG/I ntrasite. Bactroban. Diarrhoea Kaolin 10mls tds [Adsorbant] Lomotil / tds-qds [Antimotility]

Loperamide (Imodium) 2-4mg tds-qds [Antimotility] Diabetes/Hypogl ycemia Acarbose(Glucoba y) 50-100mg omtds Glibencamide(Dao nil) 2.5-15mg om[long act su] [CI:>60yrs] Gliclazide(Diamicr on) 40-80mg om/bd [short act su,2nd gen] Glipizide (Minidiab) 2.5mg10mg om/bd [2nd gen su] Metformin 250mg1g om-tds [CI:ESRF,acidosis] (1st line in fat pt) Metformin (Glucophage) Retard 850mg bd Tolbutamide 0.51g om/bd [short act 1st gen su] Insulin: R=SI,Actrapid[yell ow bottle,clear] [short] N=Insulatard[gree n,cloudy] [intermediate]. Mixtard usu 30/70 (R:N) DKA: SI 6-10u i/v x1. 50U SI in 49.5ml N/S(1U/ml) at 6mls/hr then change N/S above to D5% at 3mls/hr once BSL<12. Hydrate with N/S 2L/2h + add K+ 20-40/hr if pu Hypoglycemia <3: Sugar drink. < 2.5: 20-40mls D50% i/v, dilute

with N/S or H20. Failed i/v: Glucagon 1U im Gastritis/Bleedin g GIT/PUD Antacid / bd-tds po Famotidine 20mg bd po [with NSAIDs] Mist carbinimative 10mls tds/prn po [wind] MMT 10mls tds/qds/prn po Omeprazole(Losec )/Pantoprazole 20mg om/bd, 40mg om i/v Omeprazole infusion 8mg/h (80mg in 1 pint N/S @ 50mls/h) Somatostatin 0.25mg i/v stat then 0.25mg/h infusion(Varices). Gout Allopurinol 100300mg om [CI:acute attack] Colchicine 0.5mg 1-2h max 6mg/d or n+v/diarr/no pain then 0.5mg tds Diclofenac(Voltare n) 25-50mg tds po/75mg i/m x1 Indomethacin 2550mg tds. [Not aspirin] Hypertension Comorb:Angina/A MI: Ace/Beta/Ca. CCF: Ace+Diur. DM: Ace C/I: Ace:Cr>300, B:Asthma,Heartblk, dyslipid, C: dyslipid

Amlodipine(Norva sc) 2.5-10mg om po[Ca2+] Atenolol 50100mg om po [B] Captopril 12.525mg bd po[ACE] Enalapril 2.510mg om po[ACE] Frusemide(Lasix) 20-40mg om-bd po/i/v bolus[loop D][+ K+] Hydrochlorthiazide 25-50mg om po[Thiaz D] (elderly)[+ K+] Nifedipine(Adalat) 5-10mg om-tds po,LA 30mg om po[Ca2+] Propanolol 80160mg bd po, 1mg over 1 min max 5mg i/v[B] Spironolactone 100-200mg om po[K+sparing D] Hypt Emergency/Urgen cy (>230/130). Aim 160/100 slowly Nifedipine 10mg po 8h +/- Atenolol Nausea, Vomitting, Giddiness Maxalon 10mg tds/prn po, i/m, i/v Odansetron 4mg i/v Stemetil 5-10mg bd/tds po, 12.5mg i/m Stugeron / tds/prn po Neuro-psych meds Diazepam (Valium) 2-5mg po, 5mg i/v

Fluoxetine (Prozac) 20mg om po Haloperidol 1.5-3 8h po, 2-10mg max30 i/m Madopar 62.5mg bd po x 3/7 then up to 250mg bdtds as tol Midazolam (Dormicum) 7.5mg(tab) po,5mg i/v or im Overdose [drug tox=LiH(green tube), levels=plain] Lavage [<2h,send tox], Activated charcoal 50g 4-6h po[<4h] Paracetamol: Nacetylcysteine 150mg/kg in 200mls D5 over 30min(usu from A&E) then 50mg/kg in 1 pint D5 over 4h then 50mg/kg 1 pint D5 over 8h. Pain Paracetamol 0.51g tds-qds/prn po, 325mg supp Anarex (Paracetamol+Orp hendarine) / tds/prn [SGH] NSAIDS: With Antacid/Cimetidin e/famotidine 20mg bd Diclofenac(Voltare n)50mg tds, 75mg i/m max bd & 2/7 Indomethacin 2550mg tds po + antacid [gout] Mefenamic acid(Ponstan) 250-

500mg tds/prn po + antacid Naproxen (Synflex) 550mg bd/prn po Opioids: With Laxative (Senna/Lactulose) + Maxalon 10mg Buprenorphine(Te mgesic) 0.2-0.4mg tds-qds s/l Codeine phosphate 1530mg tds po + laxative Durogesic(Fetanyl ) patch 2550microg/h over 72h [CD] Mist Morphine 515mg 4-6h po + laxative & maxalon Morphine 0.52mg/h i/v or 25mg/h s/c (AMI: 24mg/5min) Pethidine 2575mg tds/prn i/m + maxalon 10mg i/m 4-6h Tramadol 50100mg tdsqds/prn po + lactulose Misc: Supp: Voltaren 25mg, Paracetamol 325mg (kid 125mg) Colic: Hyoscine (Buscopan) 1020mg tds po, 20mg(1ml ) i/m Topical: Faustum/Voltaren gel Piles Daflon / tds x 4/7 then / bd x 4/7 then / bd Fybogel / bd + Lactulose 10ml

tds,Lignocaine gel prn Potassium Low: Inverted T,U wave, PR elevation, ST depression Stop diuretics, glucose. <2.5: potassium 7.45% 10mls in 100ml N/S i/v over 1hr max 20mmol/h, max 20mmol/pint, do not flush Mist KCL 10mls tds po Span K 0.6-1.2g om po (also give with diuretics) High: >6 ECG:Tall T,wide QRS, small P Resonium 15g 8h po/ 30g fleet Glucose 50% 40mls(dilute w/ N/S) + insulin 6U i/v Calcium gluconate 10% 20mls slow i/v (cardioprotect) Renal

1-alpha calcidol 0.25-1mcg 23x/wk po Calcium carbonate(Calcich ew) 625mg-1.25g tds w/ meals po Ferrous fumarate 200-400mg om-bd po Renalvite / om po Eprex (Erythropoeitin) 2000-4000u 13x/wk s/c Sodium True Na+ = Na+ + gluc/4 Low:. max by 10mM/24h Not dry, renal fn good or SIADH: Fluid restrict, Frusemide Dry: 0.9% N/S 0.6*wt*[]125Na+]/154 litres / 24h <120/Fitting: Na+ 3% + Lasix [3%=514/L instead of 154]

NaCl 600mg (10mmol @) po Vitamins/Food Calcitonin 100u om i/m(test dose 0.1ml s/c) x 5/7, nasal spray (200U) / each nostril om [sitting up, 1 hour before breakfast] Ca++: Ca et vit D / om/bd po. See also Calcium. Fe: Ferrous fumarate 100400mg om/bd po +/- laxative Fe: Sangobion/Neogob ion / om/bd po Folate 10mg om po Neurobion / om/bd Vit B Co / bd Vit C: 100-200mg om/bd po, 100mg/ml i/m Vit K: 10mg om i/v x 3/7 for raised PT Vitamin cocktail 5ml in each pint i/v drip

Thiamine (Vit B1) 10-30mg po, 100mg om i/v (alcoholic) Enteral/NG feed 1kCal = 4 kJ. Avg=15002500kcal/d Ensure: 1000kJ/250mL Ensure Plus: 1250kJ/200mL Glucerna: For DM. 1kCal/mL. 6 cans = 1.42L/d Promod (Protein) 5-6 scoops/d Common calculations CreatinineClear (ml/min) = (140Age) x Wt [72 x Cr/38.4], Weight: 1 kg = 2.2 lb Glucose: mmol/L = mg/dl * 0.055 Length: 1 cm = 0.394 in = 0.0328 ft Temperature:Celsi us=5*(Farenheit32) / 9

COMMONLY USED ABBREVIATIONS IN NEUROSURGERY SGH ACA A1 A2 ACOM AICA BG CPP EVD EDH FM 4VA Gamma Knife GBM ICH ICP IVH Anterior Cerebral Artery 1 segment of ACA after ICA bifurcation 2nd segment of ACA after ICA bifurcation Anterior Communicating Artery Anterior Inferior Cerebellar Artery Basal Ganglia Cerebral Profusion Pressure External Ventricular Drain Extra Dural Hematoma Face Mask FOUR Vessel Angiogram (2 Carotids + 2 Vertebrals) Stereotactic Radio Surgery GlioBlastoma Multiforme IntraCranial Haemorrhage IntraCranial Pressure IntraVentricular Haemorrhage
st

ICA Internal Carotid Artery I/O Input and Output of fluids IA LINE Intra Arterial LINE LD Lumbar Drain LP Lumbar Puncture LOW/LOA Loss of Weight/ Loss of Appetite MAP Mean Arterial Pressure MCA Middle Cerebral Artery M1 1st segment of MCA from ICA M2 2nd segment of MCA in the Sylvian Fissure NICU Neurosurgical Intensive Care Unit PCA Posterior Cerebral Artery st P1 1 segment of PCA after Basilar bifurcation P2 2nd segment of PCA after Basilar bifurcation PCOM Posterior Communicating Artery PICA Posterior Inferior Cerebellar Artery SAH SubAracnoid Hemorrhage SDH Sub Dural Hematoma TCD TransCranial Doppler Ultrasound TM Tracheostomy Mask T1 1st Thoractic Vertebrae T2 2nd Thoractic Vertebrae T3 3rd Thoractic Vertebrae TRIPLE H THERAPY Hemodilution, Hypertension and Hydration Therapy VA Vertebral Artery VP SHUNT Ventriculo Peritoneal Shunt VES Video assisted Endoscopic Sympathectomy WBRT Whole Brain Radiotherapy

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