Surgery (I) Log Book

SURGERY (I) LOG BOOK
KING FAISAL UNIVERSITY
COLLEGE OF MEDICINE IN AL-AHSSA

4TH YEAR MEDICAL STUDENT
WRITTEN BY: QASIM HUSSAIN AL-HALEIMI
Group: B3
AC:207002113
2010
CONTENTS:
-Summary of the Log Book.
-CASES (PRESENTED & NON-PRESENTED) In all weeks.
-BEDSIDE TEACHINGS & KEYNOTES.
-SURGICAL SKILLS.
-ASSIGNMENTS & RESEARCHES.

COLLEGE OF MEDICINE IN AL-AHSA
CLASS IV YEAR
LOG BOOK FOR HOSPITAL ROTATION
SUMMARY
1. No. of Patients examined : 13
2. No. of case histories presented : 13
3. Ward Attendance : All attended
4. No. of assignments completed : All assignments
5. Lectures attended : All lectures
Name & Signature of faculty : Name & signature of student:
Qasim Hussain AL-Haleimi

SURGICAL CASES
1st Round
COLLEGE OF MEDICINE
IN AL-AHSSA
NAME: QASIM HUSSAIN AL-HALEIMI

Group : B3
AC:207002113
Supervised by Dr. Mohammad Atif Khan

Case#1 Date: 23-05-2010 Sunday
Personal : Smaher is 16 year old female Saudi patient from AL-Jaffer studying in the third class intermediate
school.
Diagnosis: Sickle cell Anemia Vaso-occlusive Crisis.
Summery of the case:
The patient is a known case of SCD. She was admitted to the hospital last Friday complaining of a pain in
the shoulders & the low back which is progressive continuous only relieved by taking analgesics. There
were no menstrual abnormalities. The patient was treated with analgesic & normal saline for hydration. No
investigation were implemented in the hospital. No any surgical interventions as splenectomy,
cholecystectomy, or hip replacement.
Case# 2 Date: 25-05-2010 Tuesday
Personal: My patient is 37 year old Saudi male patient admitted to the hospital complaining of a swelling in
the upper left back.
Diagnosis: Lipoma
Summary of the case:
The patient was in his usual state of health till one month prior to admission when his wife started noticing a
swelling in the back which is nontender but when palpated a while it leads to redness in that area & the
patient notice some hotness. The lump was fixed with slowly enlargement. No history of any chronic
medical illness,no history of blood transfusion. Regarding family history his father had bladder cancer. No
drug history.On examination the lump borders are not clear the swelling is 8*6*3 cm in the left sub scapular
region. Semisolid to hard the surrounding skin is normal with no pigmentations. smooth surface, no sign of
inflammation, no limitation in movement. The lump is prominent when bending forward or to the lateral
side & diminished, or hidden when relaxing the muscles of the back. The patient was referred to surgery
ward for lump excision.
Case#3 Date: 25-05-2010 Tuesday
Personal: My patient is 21 year old Saudi male patient studying in college of technology in AL-Ahssa
admitted to the hospital complaining of an swelling in the foot specially in the left big toe.
Diagnosis: Foot swelling.
The patient was in his usual state of health till week prior to admission when he noticed a lump in the big toe
of the left foot. With no history of trauma, or accident. The patient was investigated for DM but it was
normal.
Case# 4 Date: 25-05-2010 Tuesday
Personal: My patient is 17 year old Saudi female patient. She is studying at secondary school admitted to the
hospital complaining of neck swelling & pain.
Diagnosis: Hyperthyroidism
She was in her usual state of health till 40 days prior to admission when she started to develop pain in the
neck with rapid weight loss then 20 days later she started to notice swelling in the neck that was diffuse with
ill defined margins, with no redness, she was admitted to the hospital as having hyperthyroidism for
investigation, & she was to be sent to KFH for imaging studies of the neck. On brief examination her mother
refuse to complete the examination because she will go to the KFH for evaluation of the case. But on
inspection bulging of the eye was easily noticed with sweating in the hands & some tremors in the extended
hand suggesting Graves’ disease.
Case#5 Date: 25-05-2010 Tuesday
Note: we have take short history & focused examination because the patient was so busy & she wants to go
Personal:
Female Saudi patient living in Al-Jaffer 32 year old admitted through OPD complaining of multiple swelling
in the scalp.
Diagnosis: Sebaceous cyst.
Because the patient refuses to show her head we take permission to see only one swelling.
It was normal in temperature, non tender, firm to hard, well defined edges, smooth surface, with centralized
brownish punctum.
Case#6 Date: 29-05-2010 Saturday
Personal: Aqeel is 23 years old, Saudi male patient, living in Al-Hassa, married without children, non-
smoker.
Chief complain:
The patient admitted through ER since 1 day complaining of fever, swelling at the lateral side of neck with
pain in the throat 2 days prior to his admission.
Diagnosis: Pharyngitis
HPI:
The patient was in his usual state of health till 2 days prior to his admission when he started to complain of
fever with chills, swelling at the lateral side of neck and pain in the throat. The fever started at Wednesday
with some drowsiness, it measured about 38.9 C. Then followed by pain and swelling at the lateral side of
neck at Thursday .The pain was acute in onset, continuous and stationary, aggravated by cold weather, and
relived by analgesic drug. No his of trauma to the neck. No signs of thyrotoxicosis.
Past history:
No history of similar attack. No history of medical or surgical illnesses. No history of blood transfusion.
Drug history:
Analgesic & Antibiotics.
Family history:
His parents have DM and HTN.
Social history:
Examination of swelling:
Inspection:
By inspection there is no swelling prominent in the neck. Inspection of the oral cavity shows prominent
redness a long the pharynix which suggest inflammation.
By palpation:
One swelling in the lateral side of neck deep lymph nodes, non-tender, ill define margin, firm, about 5x5 cm,
no redness, fixed to muscle.
Case#7 Date: 30-05-2010 Sunday
Personal: Ali Mohammad A-Mater, is a 17 year old, Saudi male patient, single, living in Al-Sbbat which is a
village in Al-Hassa, student in intermediate school, non-smoker.
Chief complain:
The patient admitted through ER 1 day ago C/O abdominal pain few hours prior to his admission.
Diagnosis: Abdominal pain under investigation
HPI:
The patient is a known case of SCD. The patient was in his usual state of health till few hours prior to his
admission when he started to complain of diffuse abdominal pain. The pain was precipitated by abdominal
trauma. The pain was sudden in onset, intermittent and progressive, compressive in character, graded as 5/10
in severity, relieved by resting and drugs and aggravated by walking. The pain is not associated with
vomiting, heartburn, diarrhea, constipation, loin pain, dysurea, hematurea. No crisis pain. No fever, no
sweating, no weight loss, no loss of appetite.
Past history:
The patient is a known case of SCD since childhood.
No history of blood transfusion.
No previous hospitalization like this time.
The patient had a frequent hospitalization for SCD VOC 1 -2 every year.
Drug history:
Folic acid.
Analgesic drugs.
IV nutrition.
Morphine
Family hisrory:
Father & mother is SCD. Relatives.
Review of system:
No significance.
Examination of the abdomen:
Mild splenomegaly around 2-3 cm below the costal margin.

SURGICAL CASES
2nd Round
COLLEGE OF MEDICINE
IN AL-AHSSA

Group : B3
AC:207002113
Supervised by
Dr.Nabeeh Mararr
Not Presented
CASE # 1 Trauma in the Abdomen Date: 05-06-2010 Saturday
Personal : Sarah is a 27 year old female Saudi patient living in AL-Oyuon, married with 3 offsprings, she is
pregnant in the 4th month ,with no special habits of clinical importance, admitted to the hospital 1 day ago
(04-06-2010).
CC: She was presented to the ER with a history of trauma 1 day ago
Diagnosis: Acute Abdomen
The patient was in her usual state of health till yesterday when she had a fight with her husband, that
develops bruises in the face associated with pain in the abdomen which is generalized that latterly becomes
localized in the upper right quadrant of the abdomen this pain was sudden in onset,continuous , progressive
dull aching, compressing in character which is severe, not exacerbated by anything & relived by analgesic
drug. Because she was pregnant ultrasound was done for the health of her baby.
Hospital course: She was treated in the hospital by IV fluids, analgesic drugs, folic acids & iron for her
pregnancy.
Ultrasound of the fetus & abdomen.
Presented Clinical Cases
Case#1 Acute abdomen Date: 05-06-2010 Saturday
Personal: Yaqoub is 31 year old Saudi male, single, living in AL-Oyuon, working as secretary in company,
and smoker. Admitted to the hospital 1 day ago
Diagnosis: Crohn's disease.
Chief Complaints:
Abdominal pain in lower right side of the abdomen & diarrhea 2 days ago
Summary:
The patient is a known case of crhons disease. He was in his usual state of health till 2days prior to his
admission when he started to develop an abdominal pain which is acute in onset, continuous and stationary,
compressing, severe ( scale 10/10), aggravated by effort, with no reliving factor, associated with nausea,
without vomiting, diarrhea, chest pain and loss of consciousness.
Past history:
No DM, HTN. There is a history of hemorrhoid, 8 years ago, blood transfusion, 3 years ago.
Drug history:
Mesalazine, 400mg, 3 times/day
Family history:
father has DM and died by renal failure, his brother has DM.
Social history:
Mild Smoker
Review of system:
CNS: mild headache
CVS: chest pain, palpitation.
CASE# 2 Acute abdomen Date: 06-06-2010 Sunday
Personal: Huthifa Al-Kulaib, is an 18 year old Saudi male secondary school student living in AL-Oyuon,
single, with no special habit of clinical importance, Admitted to the hospital in the same day of history
taking(06-06-2010).
Diagnosis: Appendicitis.
C.C: Diffuse abdominal pain especially at the lower right side of the abdomen 1day ago.
He was in his usual state of health till a day prior to his admission when he eats from restaurant he started to
develop generalized abdominal pain which is, sudden in onset, continuous and progressive, not radiated,
Dull ache, severe (6/10), relived by bending forward and flexing the knee, aggravated by pressure on the
Right lower quadrant of the abdomen, this pain is associated with nausea and vomiting. No dyspagea, no
diarrhea, no constipation, no fever.
Past history:
No chronic diseases, no any surgical interventions
Drug history:
Anti-allergic drug 2 tablet/day
Dermatological drug
Family history:
Father and Mother have HTN and DM.
Social history:
Living with his family
Examination:
-Right iliac fossa tenderness.
-No fever.
SURGICAL CASES
3rd Round
COLLEGE OF MEDICINE
IN AL-AHSSA
GROUP: B3
AC: 207002113
SUPERVISED BY:
Dr.GR.VERMA
CASE # 1 Scrotal swelling, & pain in the Rt thigh Date: 12-06-2010 Saturday
Personal: Saleh AL-Hamad is a 15 years old Saudi male, living in Al-Yahia single, studing in intermediate
school and non smoker admitted through OPD clinic in PSBJH complaining of a scrotal swelling & pain in
the Rt thigh.
Admission on: 06-06-2010.
Diagnosis: Tisticular tumor, with epididmorchitis
Note: History was taken post operative (high orchiodectomy)
HPI:
The patient is a known case of SCD. The patient was in his usual state of health till around one month prior
to admission when he started to notice a swelling in the base of the scrotum while taking shower which is
solid to hard around the size of peanuts (circular to Ovale) ,not associated with diurnal variation, non
tender, fixed to the scrotal skin with no local redness, and not associated with urinary disturbances as
dysuria, hematuria, frequency micturation, this swelling was progressing in size from the size of peanuts in
the first to the size of lime prior to admission. The patient also complain of a pain in the right thigh which is
insidious in onset progressive stabbing in character moderate to severe graded as 6 out of 10 awaken the
patient from sleep, not associated with fever, exacerbated by effort, & adduction of the leg near to the
scrotum & relieved by taking analgesic medication.
Past history (Medical & Surgical):
-No similar attack previously.
-SCD. When he was child hospitalization 1 every 3-4 months
-No splenectomy, or cholecystectomy.
-No
-Tonsilectomy. When he was a child
Drug history:
-No drug allergy.
-Larotidine. 3 days
-Folic acid as needed from birth for SCD.
Family history:
-Consinguinous marriage.
-No chronic diseases in the family.
Social history:
-The patient is in a moderate socioeconomic status living with his family in good brand new house.
Systemic review : no significant problem.
Hospital course:
-CBC, Blood analysis, Hb electrophoresis.
-Urinalysis.
-Abdominal ultrasound.
-Chest x-ray.
-MRI of the pelvis & right leg he will be sent to KFH.
Non- presented
CASE# 2 ANAL FISSURE Date: 15-06-2010 Tuesday
Personal: Ali Tofiq AL-Hazam is 36 year old Saudi male, married and has 3 offspring living in abu sahbal
(North AL-Mobaraz) working as prisoner. He was referred from Al-mobaraz health center to PSBJH last
Sunday. He was admitted in the hospital complaining of anal bleeding & pain.
HPI:
The patient was in his usual state of health till around one year when he started to notice pain while
defecating, this pain was chronic for around one year stationary in onset compressing in character so severe
graded as 8 out of 10 aggravated by defecation, & setting and relieved by standing & taking analgesic drugs
locally as suppositories this pain, this pain was associated with per rectal bleeding, bleeding occurs with &
without defecation, it is also associated with itching in the perianal area, it is not associated with fever,
hematuria, conistipation, diarrhea, or dysuria.
Past history:
-Inguinal hernia about 10 years.
-No similar condition in the past.
Drug history:
-Voltarin 50 mg per day.
-Metronidazole for itching per anally 500 mg per day.
-Xylosine ointment.
Family history:
Mother & father are DM, & HTN.
Social history:
The patient is living in good socioeconomic status with his family.

SURGICAL CASES
4th Round
COLLEGE OF MEDICINE
IN AL-AHSSA

Group : B3
AC:207002113
Supervised by Dr. Ossama Zakaria

Case#1 Date: 19-06-2010 Saturday
Personal: Gadah abdulaziz AL-Zaid is 32 year old Saudi female living in Al-Rashidiah and working as
volunteer woman
She started her menarche when she was 13 & it is regular.
Chief Complaints: Abdominal pain, vomiting, & fever.
Diagnosis: Appendicular mass, Terminal ileitis, peritonitis, & distal colitis.
HPI: The patient was in her usual state of health till 8 days prior to admission when she started to develop an
abdominal pain in the upper right side of the abdomen which is gradual in onset continuous & progressive
not radiated to any site so severe that interfere with her daily work described by the patient as dull aching,
associated with burning sensation a long the sternum, 3 times vomiting of food content which is acidic,
sometimes there is diarrhea, exaggerated by taking food, & relieved by taking medications , this pain is not
associated with her menstrual period, there is no burning micturation, no dysurea, no pelvic discharge.
Past History:
She had a previous similar attack 8 years ago.
Post traumatic limb fracture 2 years ago
She had a previous hospitalization for appendicitis around one month with suspicion to do appendectomy.
Drug history:
Antibiotics.
IV nutrition.
Family history:
No diseases in the family.
Menstrual History:
No pain during menstruation, normal amount of blood for around a week,no irregularities.
Social history:
Poor socioeconomic status.
SR:
Appendicular mass, patient looks in pain, enlarged sigmoid colon due to feces.no other significant sign.
BEDSIDE TEACHING &
KEYNOTES
COLLEGE OF MEDICINE
IN AL-AHSSA

Group : B3
AC:207002113
SCD
History,Examination, Investigation, & Treatment or Management
History:
-Personal Information: name,age,gender,occupation,marital status,consinguinus marriage,day of

admission,Residency,take the premarriage testing.
Chief complaints:
The two major problems that brought the SCA patient to the hospital are:
1-Hemolytic anemia.
2-Tissue infarction due to vaso-occlusion (Which is the most common).
Usually the SCD patient come with one or two of these complaints:
Long-term complains due to hemolysis:
-Generalized fatigue.
-Increased susceptibility to infections (chest infection as pneumonia ,meningitis,osteomyelitis).
-Leg ulcers due to ischemia.
-Gallstones so some patient are having cholecystectomy.
-Aseptic necrosis of bones specially femoral head so patient may present with hip or pelvic pain.
-Blindness due to retinal detachment.
-Chronic kidney disease due to vascular abnormalitiy.
-Bossing of the skull and sometimes the sternum as a compensatory mechanism in infantile age to less than one year
of age.
Infarctions due to vaso-occlusion:
-Bone pain is the most common problem patients come with. It defer in child as well as in adults. In child the most
common bones affected are fingers & toes, while in adults legs,arms, and sometimes the back & the chest.
-Spleen infarction or autosplenectomy and spleenomegaly.
-Kidney disease presenting as hematuria which is more common in SCT leading to papillary necrosis of the renal
calysis.
-Mesentaric infarctions are not so common but may occur presented as acute abdomen.
-Chest pain is almost common due to pulmonary infarctions which may be exacerbated by dehydration, chilling, &
chest infection mainly streptococcus penumoniae.
-CNS stroke or Transient ischemic attack (TIA) may occur in thrombosis.
-Penile disease known as priapism (Painfull erection) due to blockage of corpora cavernosa.
Other manifestations not specific includes:
-Hepatomegaly.
-Jaundice.
-Delayed puberty.
-Non-healing ulcers in the legs.
History of the Presenting illness: detailed description of the patient complaints regarding:
-Site, onset, duration, pattern, course, character, severity, radiation, associated symptoms, relieving factors, &
exacerbating factors.
Negative signs should be presented.
Past medical & surgical history:
-Any previous attack similar to this condition.
-Hip replacement.
-Cholecystectomy.
-Chest infection.
-Cardiac disease.
-Infectious diseases(malaria,& schestosomiasis, hepatitis).
-Endocrine disorders (Thyroid, or pituitary disease).
-Kidney disorders.
- Blood transfusion.
-Bone marrow transplantation.
-Splenictomy.
Drug History:
-History of drugs that cause hemolysis:
Extravascular Hemolysis
-Alpha-methyldopa & levodopa
-Diclofenac
-Ibuprofen
-Interferon alfa
-Mefenamic acid
-Penicillin(Carbenicillin,ampicillin,& methicillin)
-Procainamide
Intravascular Hemolysis:
-Acetaminophen
-Chlorpromazine
-Fluorouracil
-Hydrochlorothiazide
-Hydralazine
-Insulin
-Isoniazid
-Melphalan
-Phenacetin
-Probenacid
-Quinidine & Quinine (treatment for malaria).
-Rifampin
-Streptomycin
-Sulfonamides
-Sulindac
-Tetracycline
History of addicting analgesic drugs as morphine.
History of folic acid tablet which increase RBCs production as compensatory mechanism.
Family history:
-Genertic disease in the family.
-History of multifactorial disease.
-Consinguinus marriage.
-History of sudden infantile death.
Social history:
Living where, hows taking care of you, especially during the attack. How much your fond per month. Educational
level of the patient & his/her parents. Smoking , or alcohol.
Menstrual history:
Regular, disturbed, normal amount of blood, painfull menses (Dysmenorrhea) , last period, stoppage of menses in
elderly when (Amenorrhea) , pregnancy.
Review of systems:
General:
-Posture of the patient usually is important indicating pain.

-Hair distribution
-Eye discolorations:
Jaundice 80-90% of the SCA patients have at least a mild degree of jaundice.
Pallorness.
Red eye in conjunctivitis.
-Skin turger as a mild degree of dehydration.
-Generalized fatigability.
-Vital signs: (RR, BP, P, & TEMP).
-Look for cyanosis.
-Carotid pulses,& JVP.
-Localize the apex beat.
-Look for clubbing.
RS:
-Chest shape.
-Trachea.
-Breath sounds.
-Detection of any adventitious sounds.
CVS:
-Palpation:
Carotid, suprasternal , epigastric , aortic , pulmonary, tricuspid, & mitral areas.
-Auscultation: S1,S2, splitting between aortic & pulmonary sounds with respiration.
-Any additional murmer and localize it in systole or diastole.
GI:
-Ask for any GI symptoms as constipation,diarrhea,vomiting,hematemesis,melena,heartburn,dyspepsia,dysphagia.
Inspection:
-Look for the abdomen shape (Countor) ,localize the umbilicus, look for the oral cavity ouder ,hygiene, whitish
discoloration of the cavity which suggest oral candidiasis, look below the tongue for cyanosis, look to the abdomen for
hernia femoral, inguinal, diaphragmatic,& umbilical. Look for scars, dilated veins.
Palpation:
Superfecial palpation for swelling & tenderness.
Deep plapation for organs liver,spleen,& kidneys.(Look for splenomegaly or hepatomegaly)
Percussion:
Liver span
Ascultation:
Intestinal prestalesis.
Aortic bruit.
Renal bruit.
GUS: ask for urine frequency & color ,micturation pain, pripism(Painfull erection).
MS: ask for screening exam GALS(Gait, Arms, Legs, & Spine) for inspection ,palpation , & movements specially legs
& arms.
CNS: Ask the patient to walk around the room for gait assessment, perform cranial nerve examination, motor &
sensory system examination.
Investigations :(Lab,Imaging,&Biopsey)
Laboratory:
-CBC, WBC, DLC, Reticuocyte count.
-Liver function tests.
-LDH.
-Bilirubin assy.
- Hemoglubin electrophoresis HbF should be less than 40%.
-Urinalysis for urobilinogen mainly.
-Sickling test.
Imaging:
-Chest x-ray for chest infection consolidations.
-Abdomenal Ultrasound for hepatomegaly, splenomegaly, biliary obstruction.
Treatment or Management:
Treatment of the acute case by:
-Hydration.
-Oxygenation by ventilation.
-Blood transfusion or exchange.
-Antibiotic as needed.
-Analgesia.
-Histamine receptor antagonist for itching.

Treatment as a chronic case:
-Hydroxyurea.
-Folic acid.
-Penicillin as preventive measure.
-Cholestyramine
In children :
-Bone marrow transplantation is effective.
Under research:
-Gene therapy.
-Stem cells.
-Phytochemicals like Nicosan the same antisickling effect as hydroxyurea.
Vaccination for the Encapsolated organism mainly salmonella, Pneumococcal, Meningococcal, Hemophilus
influanzae & chlamydial organism.
Major cause of death:
-Acute chest syndrome.
-TIA & Stroke.
-Coronary syndrome.
Date: 23-05-2010
COMPLICATIONS :
 Overwhelming post-(auto)splenectomy infection (OPSI), which is due to functional asplenia,

caused by encapsulated organisms such as Streptococcus pneumoniae and Haemophilus influenzae.
Daily penicillin prophylaxis is the most commonly used treatment during childhood, with some
haematologists (hematologists) continuing treatment indefinitely. Patients benefit today from routine
vaccination for H. influenzae, S. pneumoniae, and Neisseria meningitidis.
 Stroke, which can result from a progressive narrowing of blood vessels, preventing oxygen from
reaching the brain. Cerebral infarction occurs in children and cerebral hemorrhage in adults.
 Cholelithiasis (gallstones) and cholecystitis, which may result from excessive bilirubin production
and precipitation due to prolonged haemolysis.
 Avascular necrosis (aseptic bone necrosis) of the hip and other major joints, which may occur as a
result of ischemia.
 Decreased immune reactions due to hyposplenism (malfunctioning of the spleen).
 Priapism and infarction of the penis.
 Osteomyelitis (bacterial bone infection); the most common cause of osteomyelitis in sickle cell
disease is Salmonella (especially the non-typical serotypes Salmonella typhimurium, Salmonella
enteritidis, Salmonella choleraesuis and Salmonella paratyphi B), followed by Staphylococcus
aureus and Gram-negative enteric bacilli perhaps because intravascular sickling of the bowel leads
to patchy ischaemic infarction.
 Opioid tolerance, which can occur as a normal, physiologic response to the therapeutic use of
opiates. Addiction to opiates occurs no more commonly among individuals with sickle-cell disease
than among other individuals treated with opiates for other reasons.
 Acute papillary necrosis in the kidneys.
 Leg skin ulcers.
 In eyes, background retinopathy, proliferative retinopathy, vitreous haemorrhages and retinal
detachments, resulting in blindness. Regular annual eye checks are recommended.
 During pregnancy, intrauterine growth retardation, spontaneous abortion, and pre-eclampsia.
 Chronic pain: Even in the absence of acute vaso-occlusive pain, many patients have chronic pain
that is not reported.
 Pulmonary hypertension (increased pressure on the pulmonary artery), leading to strain on the right
ventricle and a risk of heart failure; typical symptoms are shortness of breath, decreased exercise
tolerance and episodes of syncope.
 Chronic renal failure due to Sickle cell nephropathy—manifests itself with hypertension (high
blood pressure), proteinuria (protein loss in the urine), hematuria (haematuria) (loss of red blood
cells in urine) and worsened anaemia. If it progresses to end-stage renal failure, it carries a poor
prognosis.
Intravenous Fluids
Giving of liquid substances directly into a vein. For emergencies
This may be to correct dehydration or an electrolyte imbalance, to deliver medications, or for blood transfusion.
Types of fluids:
1-crystalloids
Crystalloids are aqueous solutions of mineral salts or other water-soluble molecules. Colloids contain larger insoluble
molecules, such as gelatin; blood itself is a colloid.
The most commonly used crystalloid fluid is normal saline, a solution of sodium chloride at 0.9% concentration, which is
close to the concentration in the blood (isotonic). Ringer's lactate or Ringer's acetate is another isotonic solution
often used for large-volume fluid replacement. A solution of 5% dextrose in water, sometimes called D5W, is often used
instead if the patient is at risk for having low blood sugar or high sodium.
2-colloids.
Colloids preserve a high colloid osmotic pressure in the blood, while, on the other hand, this parameter is decreased by
crystalloids due to hemodilution.However, there is still controversy to the actual difference in efficacy by this
difference. Another difference is that crystalloids generally are much cheaper than colloids.
Note: Intravenous fluids must always be sterile.
Composition of common crystalloid solutions
Solution Other Name [Na+](mmol/L) [Cl-](mmol/L) [Glucose](mmol/L) [Glucose](mg/dl)
D5W 5% Dextrose 0 0 278 5000
2/3D & 1/3S 3.3% Dextrose / 0.3% saline 51 51 185 3333
Half-normal saline 0.45% NaCl 77 77 0 0
Normal saline 0.9% NaCl 154 154 0 0
Ringer's lactate Lactated Ringer 130 109 0 0
D5NS 5% Dextrose, Normal Saline 154 154 278 5000
Ringer's lactate also has 28 mmol/L lactate, 4 mmol/L K+ and 1.5 mmol/L Ca2+. Ringer's acetate also has 28 mmol/L
acetate, 4 mmol/L K+ and 1.5 mmol/L Ca2+.
Effect of adding one litre
Solution Change in ECF Change in ICF
D5W 333 mL 667 mL
2/3D & 1/3S 556 mL 444 mL
Half-normal saline 667 mL 333 mL
Normal saline 1000 mL 0 mL
Ringer's lactate 900 mL 100 mL
Complication of IV Line
Infection
Any break in the skin carries a risk of infection. Although IV insertion is an aseptic procedure, skin-dwelling organisms such
as Coagulase-negative staphylococcus or Candida albicans may enter through the insertion site around the catheter, or
bacteria may be accidentally introduced inside the catheter from contaminated equipment. Moisture introduced to
unprotected IV sites through washing or bathing substantially increases the infection risks.
Infection of IV sites is usually local, causing easily visible swelling, redness, and fever. If bacteria do not remain in one area
but spread through the bloodstream, the infection is called septicemia and can be rapid and life-threatening. An infected
central IV poses a higher risk of septicemia, as it can deliver bacteria directly into the central circulation.
Phlebitis
Phlebitis is inflammation of a vein that may be caused by infection, the mere presence of a foreign body (the IV catheter) or
the fluids or medication being given. Symptoms are warmth, swelling, pain, and redness around the vein. The IV device
must be removed and if necessary re-inserted into another extremity.
Due to frequent injections and recurring phlebitis, scar tissue can build up along the vein. The peripheral veins of
intravenous drug addicts, and of cancer patients undergoing chemotherapy, become sclerotic and difficult to access over
time, sometimes forming a hard “venous cord”.
Infiltration
Infiltration occurs when an IV fluid accidentally enters the surrounding tissue rather than the vein. It is characterized by
coolness and pallor to the skin as well as localized swelling or edema. It is usually not painful. It is treated by removing the
intravenous access device and elevating the affected limb so that the collected fluids can drain away. Infiltration is one of the
most common adverse effects of IV therapy and is usually not serious unless the infiltrated fluid is a medication damaging to
the surrounding tissue, in which case the incident is known as extravasation.
Fluid overload
This occurs when fluids are given at a higher rate or in a larger volume than the system can absorb or excrete. Possible
consequences include hypertension, heart failure, and pulmonary edema.
Electrolyte imbalance
Administering a too-dilute or too-concentrated solution can disrupt the patient's balance of sodium, potassium, magnesium,
and other electrolytes. Hospital patients usually receive blood tests to monitor these levels.
Embolism
A blood clot or other solid mass, as well as an air bubble, can be delivered into the circulation through an IV and end up
blocking a vessel; this is called embolism. Peripheral IVs have a low risk of embolism, since large solid masses cannot travel
through a narrow catheter, and it is nearly impossible to inject air through a peripheral IV at a dangerous rate. The risk is
greater with a central IV.
Air bubbles of less than 30 milliliters are thought to dissolve into the circulation harmlessly. Small volumes do not result in
readily detectable symptoms, but ongoing studies hypothesize that these "micro-bubbles" may have some adverse effects. A
larger amount of air, if delivered all at once, can cause life-threatening damage to pulmonary circulation, or, if extremely
large (3-8 milliliters per kilogram of body weight), can stop the heart.
One reason veins are preferred over arteries for intravascular administration is because the flow will pass through the lungs
before passing through the body. Air bubbles can leave the blood through the lungs. A patient with a heart defect causing a
right-to-left shunt is vulnerable to embolism from smaller amounts of air. Fatality by air embolism is vanishingly rare, in part
because it is also difficult to diagnose.
Extravasation
Extravasation is the accidental administration of IV infused medicinal drugs into the surrounding tissue which are caustic to
these tissues, either by leakage (e.g. because of brittle veins in very elderly patients), or directly (e.g. because the needle
has punctured the vein and the infusion goes directly into the arm tissue). This occurs more frequently with
chemotherapeutic agents and people who have tuberculosis.
PORTOSYSTEMIC SITE OF ANASTOMOSIS & SHUNT
Branches of External Carotid Artery in the neck:
Course:
The external carotid artery begins at the level of the upper border of thyroid cartilage, and, taking a slightly curved
course, passes upward and forward, and then inclines backward to the space behind the neck of the mandible, where
it divides into the superficial temporal and maxillary artery within the parotid gland.
Relations:
The external carotid artery is covered by the skin, superficial fascia, Platysma, deep fascia, and anterior margin of the
Sternocleidomastoid; it is crossed by the hypoglossal nerve, by the lingual, ranine, common facial, and superior
thyroid veins; and by the Digastric and Stylohyoid; higher up it passes deeply into the substance of the parotid gland,
where it lies deep to the facial nerve and the junction of the temporal and internal maxillary veins.
Medial to it are the hyoid bone, the wall of the pharynx, the superior laryngeal nerve, and a portion of the parotid
gland.
Lateral to it, in the lower part of its course, is the internal carotid artery.
Posterior to it, near its origin, is the superior laryngeal nerve; and higher up, it is separated from the internal carotid by
the Styloglossus and Stylopharyngeus, the glossopharyngeal nerve, the pharyngeal branch of the vagus, and part of
the parotid gland.
Branches:
Arising in carotid triangle
-Superior thyroid artery
-Ascending pharyngeal artery
-Lingual artery
-Facial artery
-Occipital artery
-Posterior auricular artery
Terminal branches
Maxillary artery
Superficial temporal artery

FUNCTIONS OF RECURRENT LARYNGEAL NERVE
Introduction:
The recurrent (inferior) laryngeal nerve is a branch of the vagus nerve (X) that supplies motor & sensory function to
the larynx (voice box). It travels within the endoneurial sheath. It is referred to as "recurrent" because the branches of
the nerve innervate the laryngeal muscles in the neck through a rather circuitous route: it descends into the thorax
before rising up between the trachea and esophagus to reach the neck.
The left laryngeal nerve loop under and around the arch of the aorta (ligamentum arteriosum) before ascending,
whereas the right loops around the right subclavian artery
It supplies all laryngeal muscles except for the cricothyroid, which is innervated by the external branch of the
superior laryngeal nerve.
The recurrent laryngeal nerve enters the pharynx, along with the inferior laryngeal artery, below the inferior constrictor
muscle to innervate the Intrinsic Muscles of the larynx responsible for controlling the movements of the vocal folds.
Clinical significance:
The nerve is known for its importance in thyroid surgery, as it runs immediately posterior to this gland. If it is
damaged during surgery, the patient will have a hoarse voice. Which can be assessed by laryngoscopy, during
surgery by confirming the absence of movement in the affected side of the vocal cords.
-Similar condition can occur in tumor nerve invasion, or trauma to the neck with clinical picture of paralysis of the vocal
cords.
-Breathing difficulties, and aphonia, or the inability to speak if bilaterally affected.
- The right recurrent laryngeal nerve is more susceptible to damage during thyroid surgery due to its relatively medial
location
THE ANAL CANAL, PER-RECTAL EXAMINATION
Anatomy of the anal canal
The gastrointestinal tract terminates in a short segment, called the anal canal. Its external margin is poorly demarcated, but
generally the skin of the anal canal can be distinguished from the surrounding perianal skin by its moist, hairless appearance. The
anal canal is normally held in a closed position by action of the voluntary external muscular sphincter and the involuntary internal
sphincter, the latter an extension of the muscular coat of the rectal wall derived from endoderm while the external is derived from
ectoderm.
The anal canal is demarcated from the rectum superiorly by a serrated line marking the change from skin to mucous membrane.
This anorectal junction (often called the pectinate or dentate line) also denotes the boundary between somatic nerve suppling
below and visceral nerve suppling above to dentate line .
Control is mainly by the external sphincter so sometimes the internal sphincter can be removed(Sphincterectomy)
THE ANATOMICAL AND SURGICAL ANAL CANALS

The anatomical anal canal extends from the level of the valves of Morgagni (dentate line) to the anal margin. For surgical
purposes, the anal canal may be regarded as that portion of the terminal intestine which extends from the level where the rectum
passes through the pelvic visceral aperture- the anorectal ring-to the the anal margin. This concept of the anal canal is more
apposite for (surgical) purposes and as the anorectal ring is above the valves of Morgagni, the surgical anal canal is longer than its
anatomical counterpart see fig 1
Techniques of Examination
For most patients the rectal examiantion is probaly the least popular segment of the entire physical
examination. It may cause discomfort for the patient, perhaps embarrassment, butif skillfully done,
should not be truly painful in most circumstances. Although you may choose to omit a rectal
examination in adolescents who have no relevant complaints, you should do one in adult patients. In
middle-aged and older persons omission risks missing an asymptomatic carcinooma. A successful
examination requies gentleness, slow movement of your finger, a calm demeanor, and an explanation
to the patient of what he or she may feel.
Male
The anus and rectum may be examined with the patient in one of several positions. For most purposes, the side-lying position
is satisfactory and allows good visualization of the perianal and sacrococcygeal areas. This is the
position described below. If you suspect a cancer high in the rectum, the lithotomy position may
help to bring it into reach. By placing your opposite hand on the patient’s abdomen you can also
perform a bimanual examination in this position, thus delineating a pelvic mass.
Ask the patient to lie on his left side with his buttocks close to the edge of the examining table near
you. He should flex his legs at hips and knees. Drape the patient appropriately and adjust the
lighting for good visuallization of the anus and surrounding area. Put a glove on your right hand.
With your left hand spread the buttocks apart.
Inspect the sacrococcygeal and perianal areas for lumps, ulcers, inflammation, rashes, or excoriations. Adult perianal skin is
ormally more pigmented and somewhat coarser than the skin over the buttocks. Palpate any abnormal areas, noting lumps or
tenderness.
Lubricate your gloved index finger, explain to the patient what you are going to do, and tell him that the examiantion
maymake him feel as if he were moving his bowels but that he will not do so. Ask him to strain down. Inspect the anus, noting
any lesions.
As the patient strains, place the pad of your lubricated and gloved index finger over the anus. As the sphincter relaxes, gently
insert your fingertip into the anal canal, in a direction pointing towards the umbilicus.
If you feel the sphincter tighten, pause, reassure the patient, and, when in a moment the sphincter relaxes proceed.
Occasionally an acutely tender lesion such as an anal fissure prevents you from completing your examination. Do not try to
force it. Local anaesthesia or consultation may be necessary.
Insert your finger farther into the rectum so that you can examine as much of the rectal wall as possible. Palpate in sequence the
right lateral, posterior, and left lateral surfaces, noting any nodules or irregularities. Then turn your hand so that your finger can
examine the anterior surface and the prostate gland. Tell the patient that you are going to feel his prostate gland and that it may
make him want to urinate but he will not.Identify the lateral lobes of the prostate and the median sulcus between them. Note the
size, shape, and consistency of the prostate, feel for anynodules, and note any tenderness.
If possible, extend your finger above the prostate to the region of the seminal vesicles and peritoneal cavity. Note nodules or
tenderness.Rectal lesions just beyond your fingertip can sometimes be felt by asking the patient to strain down again. Use this
maneuver if there is any suspicion of cancer.
Gently withdraw your finger, and wipe the patient’s anus or give him tissues to do it himself. Note the color of any fecal matter
on your glove, and test it for occult blood.
Female
The rectum is usually examined after the female genitalia, while the patient is in the lithotomy position. This position is essential
for bimanual palpation. If a rectal examination alone is indicated, the lateral position offers a satisfactory alternative and affords
much better visalization of the perianal and sacrococcygeal areas.
The technique is basically similar to that described for males. The cervix is usually readily felt through the anterior rectal wall.
Sometiems a retroverted uterus is also palpable. Neither of these, nor a tampon, should be mistaken for a tumor.
Common Anorectal Conditions
Anorectal fistula:
An anorectal fistula is an inflammatory tract or tube that opens at one end into the anus or
rectum and at the other end onto the skin surface (as shown here) or into another vscus. An
abscess usually antedates such a fistula. Look for the fistulous opening or openings anywhere
in the skin around the anus.
Anal fissure :
An anal fissure is a very painful oval ulceration of the anal canal, most commonly found in the midline
posteriorly, less commonly in the midline anteriorly. Its long axis lies longitudinally. Inspection may
reveal a "sentinel" skin tag just below it, and gentle separation of the anal margins may reveal the lower
edge of the fissure. The sphincter is spastic; the examination painful. Local anaesthesia may be required.
External Hemorrhoid :
Hemorrhoids are varicose veins. External hemorrhoids
originate below the anorectal line and are covered by anal skin. When uncomplicated, they may not
be visible at rest, but a thrombosed hemorrhoid presents as a painful, bluish, shiny, ovoid mass at
the anal margin. Flabby or fibrotic skin tags may mark the location of previously thrombosed or
inflamed hemorrhoids.
Internal Hemorrhoid :
Internal hemorrhoids originate above the anorectal jucnction and are covered by mucous
membrane, not skin. They are not visible unless they prolapse through the anus, nor are the soft
swellings normally identifiable by palpation. Proctoscopic examination is usually required for
diagnosis.
Prolapse of the Rectum
On straining for a bowel movement the rectal mucosa, with or without its muscular wall, may prolapse
through the anus, presenting as a doughnut or rosette of red mucosa. A prolapse involving only mucosa is
shown here. When the entire bowel wall is involved the prolapse is larger, and circular rather than radiating
folds are seen.
Polyps of the Rectum :
Polyps of the rectum are fairly common. Varying considerably in size and number, they can
develop on a stalk (pendunculated)) or lie close to the mucosal surface (sessile). They are soft
and may be difficult or impossible to feel even when in reach of the examining finger.
Proctoscopy is isually required for diagnosis, as is biopsy for the differentiation of benign from
malignant lesions.
Carcinoma of the Rectum:
Asymptomatic carcinom of the reectum makes routine rectal examination mandatory for
virtually all adults. As noted above, polypoid masses may be malignant. Another common form
of presentation is the firm, nodular, rolled edge of an ulcerated malignancy.
Peritoneal metastases:
Widespread peritoneal metastases from any source may develop in the are of the
peritoneal reflection anterior to the rectum. A firm to hard nodular rectal "shelf" may be
just palpable with the tip of the examining finger.
The Normal prostate gland :
As palpated through the anterior rectal wall, the normal prostate is a rounded, heart-shaped structure
about 2.5 cm in length, projecting less than 1.0 cm into the rectal lumen. The median sulcus can be
felt between the two lateral lobes. Only the posterior surface of the prostate is palpable. Anterior
lesions, including those that may obstruct the urthra, may not be detectable by physical
examination.
Benign Prostatic Hypertrophy :
A very common condition in men over 50 years of age, benign prostatic hypertrophy
presents as a firm, smooth, symmetrical, and slightly elastic enlargement of the gland. It
may bulge more than a centimeter into the rectal lumen. The hypertrophied tissue tends
to obliterate the median sulcus.
Carcinoma of the Prostate:
A hard, irregular nodule, producing asymmetry of the gland and a variation

in its consistency, is especially suggestive of carcinoma. Prostatic stones
and chronic inflammation can produce similar findings, and differential
diagnosis often depends upon biopsy. Later in its course the carcinoma
grows in size, obliterates the median sulcus, and may extend beyond the
confines of the gland, producing a fixed, hard, irregular mass.
Prostatitis:
The acutely inflamed prostategland is swollen, tender, and often somewheat

asymmetrical.
The gland of chronic prostatitis is variable; it may (1) feel normal, (2) be somewhat
enlarged, tender, and boggy, or (3) contain scattered firm areas of fibrosis.
Anal fissure
It is an unnatural tear in the skin of the anal canal. Anal fissures may be noticed by bright red anal bleeding on
the toilet paper, sometimes in the toilet. If acute they may cause severe periodic pain after defecation but with
chronic fissures pain intensity is often less. Anal fissures usually extend from the anal opening and are usually
located posteriorly in the midline, probably because of the relatively unsupported nature of the anal wall in that
location. Fissure depth may be superficial or sometimes down to the underlying sphincter muscle.
Causes
Most anal fissures are caused by stretching of the anal mucosa beyond its capability. For example chronic
constipation , Colonic obstruction.
Superficial or shallow anal fissures look much like a paper cut, and may be hard to detect upon visual inspection, they
will generally self-heal within a couple of weeks. However, some anal fissures become chronic and deep and will not
heal. The most common cause of non-healing is spasming of the internal anal sphincter muscle which results in
impaired blood supply to the anal mucosa. The result is a non-healing ulcer, which may become infected by fecal
bacteria.
Treatment
Non-surgical treatment is recommended as first-line treatment of acute and chronic anal fissures. Customary
treatments included warm baths, topical anesthetics, high-fiber diet and stool softeners
Classifications of anal Fistula
Goodsall rule or law:
The rule states that fistulae with an external opening anterior to a plane passing transversely through the center of the anus
will follow a straight radial course to the dentate line. Fistulae with their openings posterior to this line will follow a curved
course to the posterior midline (see image below). Exceptions to this rule are external openings more than 3 cm from the
anal verge. These almost always originate as a primary or secondary tract from the posterior midline, consistent with a
previous horseshoe abscess
Parks classification system:
The Parks classification system defines 4 types of fistula-in-ano that result from cryptoglandular infections.
 Intersphincteric
o Common course - Via internal sphincter to the intersphincteric space and then to the perineum
o Seventy percent of all anal fistulae
o Other possible tracts - No perineal opening; high blind tract; high tract to lower rectum or pelvis
 Transsphincteric
o Common course - Low via internal and external sphincters into the ischiorectal fossa and then to the
perineum
o Twenty-five percent of all anal fistulae
o Other possible tracts - High tract with perineal opening; high blind tract
 Suprasphincteric
o Common course - Via intersphincteric space superiorly to above puborectalis muscle into ischiorectal fossa
and then to perineum
o Five percent of all anal fistulae
o Other possible tracts - High blind tract (ie, palpable through rectal wall above dentate line)
 Extrasphincteric
o Common course - From perianal skin through levator ani muscles to the rectal wall completely outside
sphincter mechanism
o One percent of all anal fistulae
Hemorrhoids:
Stage 0
Morphology: Anal cushion

Symptoms:Very rare bleeding, no prolapse
Additional features: None
Visual: No increase
Age Group (years): All ages, <20 if symptomatic
Treatment: Change in bowel habit & diet, sclerotherapy / infrared coagulation for stubborn cases
Stage 1
Morphology: Small hemorrhoids

Symptoms: Intermittent bleeding, no prolapse
Additional features: None, with exception of some pain
Visual: Minor, but definite increase as can be observed by proctoscopy
Age Group (years): 20 - 45
Treatment: Sclerotherapy & Infrared coagulation. Rubber band ligation & surgery for certain cases.
Stage 2
Morphology: Intermediate hemorrhoids

Symptoms: Prolapse during straining but spontaneously return; frequent bleeding, sometimes profusely
Additional features: Anal itching (pruritus ani), and sometimes skin tags
Visual: Moderate increase of individual masses that prolapse during straining
Age Group (years): >30
Treatment: Rubber band ligation & stapling. Surgery in some cases.
Stage 3 & 4 are prolapsing hemorrhoids.
Stage 3
Morphology: Large hemorrhoids

Symptoms: Prolapse, need manual aid to put back in anal canal, bleed frequently & often profusely.
Additional features: Anal itching (pruritus ani), discomfort, skin tags
Visual: Major increase in size, prolapse
Age Group (years): > 40
Treatment: Hemorrhoidectomy
Stage 4
Morphology: Very large hemorrhoids

Symptoms: Permanent prolapse, bleed profusely, blood stains on underwear even without bowel movement
Additional features: Severe pain, anal itching, severe discomfort, soilings, skin tags
Visual: Extreme increase in size, visible skin tags, secondary hemorrhoids may develop
Age Group (years): > 50
Treatment: Hemorrhoidectomy, sometimes with anoplasty
IDIOPATHIC BOWEL DISEASES (IBD)
SIRS (Systemic Inflammatory Response Syndrome)
Definition:
SIRS was first described by Dr. William R. Nelson, of the University of Toronto, at the Nordic Micro Circulation
meeting in Geilo, Norway in February of 1983. The intent of creating an encompassing definition was to bring together
the multiple etiologies of post episode organ dysfunction (fibrin deposition, platelet aggregation, coagulopathies,
leukocyte lysosomal release) into a family of negatively synergistic responses to injury and/or infection which can
collectively lead to micro circulatory dysfunction. The implication of such a definition suggested that recognition of the
activation of one of the above noted humoral pathways suggests that additional processes are also active. The
aggregate of such pathophysiology would lead to clinical conditions such as renal failure and/or pulmonary edema.
Criteria for SIRS were established in 1992 as part of the American College of Chest Physicians/Society of Critical
Care Medicine Consensus Conference. The conference concluded that the manifestations of SIRS include, but are
not limited to:
-Body temperature less than 36°C or greater than 38°C
-Heart rate greater than 90 beats per minute
-Tachypnea (high respiratory rate), with greater than 20 breaths per minute; or, an arterial partial
pressure of carbon dioxide less than 4.3 kPa (32 mmHg)
9
-White blood cell count less than 4000 cells/mm³ (4 x 10 cells/L) or greater than 12,000 cells/mm³ (12 x
9
10 cells/L); or the presence of greater than 10% immature neutrophils (band forms)
SIRS can be diagnosed when two or more of these criteria are present.
In children, the SIRS criteria are modified in the following fashion:
-Heart rate > 2 standard deviations above normal for age in the absence of stimuli such as pain and drug
administration, OR unexplained persistent elevation for greater than 30 minutes to 4 hours. In infants, also
includes Heart rate < 10th percentile for age in the absence of vagal stimuli, beta-blockers, or congenital heart
disease OR unexplained persistent depression for greater than 30 minutes.
-Body temperature obtained orally, rectally, from Foley catheter probe, or from central venous catheter probe < 36 °C
or > 38.5 °C. Temperature must be abnormal to qualify as SIRS in pediatric patients.
-Respiratory rate > 2 standard deviations above normal for age OR the requirement for mechanical ventilation not
related to neuromuscular disease or the administration of anesthesia.
-White blood cell count elevated or depressed for age not related to chemotherapy, or greater than 10% bands + other
immature forms.
Complication:
-Acute lung injury
-Acute kidney injury
-Shock
-Multiple organ dysfunction syndrome
Causes:
The causes of SIRS are broadly classified as infectious or noninfectious. As above, when SIRS is due to an
infection, it is considered sepsis. Noninfectious causes of SIRS includetrauma, burns, pancreatitis, ischemia,
and hemorrhage.
Other causes include:
-Complications of surgery
-Adrenal insufficiency
-Pulmonary embolism
-Complicated aortic aneurysm
-Cardiac tamponade
-Anaphylaxis
-Drug overdose
Treatment:
Generally:
-Treatment underlying problem or inciting cause ( adequate fluid replacement for hypovolemia, IVF/NPO for
pancreatitis, epinephrine/steroids/benadryl for anaphylaxis). Selenium, glutamine, and eicosapentaenoic acid have
shown effectiveness in improving symptoms in clinical trials.
-Antioxidants as vitamin E.
INGUINAL CANAL
The Inguinal canal is an oblique passage through the lower part of the anterior abdominal wall. It begins at the deep
inguinal ring, which is situated in the Transversalis fascia, midway between the ASIS and the pubic symphysis, above
the inguinal ligament. The canal passes downwards and medially, to reach the superficial inguinal ring.
Deep Inguinal Ring

The deep (internal) inguinal ring is the beginning of the inguinal canal and is at a point midway between the anterior
superior iliac spine and the pubic symphysis. It is just above the inguinal ligament and immediately lateral to the
inferior epigastric vessels. Although sometimes referred to as a defect or opening in the transversalis fascia, it is
actually the beginning of the tubular evagination of transversalis fascia that forms one of the coverings (the internal
spermatic fascia) of the spermatic cord in men or the round ligament of the uterus in women.
Superficial inguinal Ring

The superficial (external) inguinal ring is the end of the inguinal canal and is superior to the pubic tubercle. It is a
triangle-shaped opening in the aponeurosis of the external oblique, with its apex pointing superolaterally and its
base formed by the pubic crest. The two remaining sides of the triangle (the medial crus and the lateral crus) are
attached to the pubic symphysis and the pubic tubercle, respectively. At the apex of the triangle the two crura are
held together by crossing (intercrural) fibers, which prevent further widening of the superficial ring.
As with the deep inguinal ring, the superficial inguinal ring is actually the beginning of the tubular evagination of the
aponeurosis of the external oblique onto the structures traversing the inguinal canal and emerging from the
superficial inguinal ring. This continuation of tissue over the spermatic cord is the external spermatic fascia.
Boundaries
Anterior Wall
The anterior wall of the inguinal canal is formed along its entire length by the aponeurosis of the external oblique
muscle. It is also reinforced laterally by the medial fibers of the internal oblique muscle because the lower fibers of
the internal oblique originate from the lateral two-thirds of the inguinal ligament. This adds an additional covering
over the deep inguinal ring, which is a potential point of weakness in the anterior abdominal wall. Furthermore, as
the internal oblique muscle covers the deep inguinal ring, it also contributes a layer (the cremasteric fascia
containing the cremasteric muscle) to the coverings of the structures traversing the inguinal canal.
Posterior Wall
The posterior wall of the inguinal canal is formed along its entire length by the transversalis fascia. It is reinforced
along its medial one-third by the conjoint tendon (inguinal falx). This tendon is the combined insertion of the
transversus abdominis and internal oblique muscles into the pubic crest and pectineal line.
As with the internal oblique muscle's reinforcement of the area of the deep inguinal ring, the position of the conjoint
tendon posterior to the superficial inguinal ring provides additional support to a potential point of weakness in the
anterior abdominal wall.
Roof
The roof (superior wall) of the inguinal canal is formed by the arching fibers of the transversus abdominis and
internal oblique muscles. They pass from their lateral points of origin from the inguinal ligament to their common
medial attachment as the conjoint tendon.
Floor
The floor (inferior wall) of the inguinal canal is formed by the medial one-half of the inguinal ligament. This rolled-
under, free margin of the lowest part of the aponeurosis of the external oblique forms a gutter or trough on which
the contents of the inguinal canal are positioned. The lacunar ligament reinforces most of the medial part of the
gutter.
Contents
The contents of the inguinal canal are:
 the spermatic cord in men;

 the round ligament of the uterus and genital branch of the genitofemoral nerve in women
 the ilio-inguinal nerve (L1)
These structures enter the inguinal canal through the deep inguinal ring and exit it through the superficial inguinal
ring.
Spermatic Cord
The spermatic cord consists of structures passing between the abdominopelvic cavities and the testis, and the three
fascial coverings that enclose these structures.
The structures in the spermatic cord include:
 The ductus deferens;

 The artery to ductus deferens (from the inferior vesical artery);
 The testicular artery (from the abdominal aorta);
 The pampiniform plexus of veins (testicular veins);
 the cremasteric artery and vein (small vessels associated with the cremasteric fascia);
 The genital branch of the genitofemoral nerve (innervation to the cremasteric muscle);
 Sympathetic and visceral afferent nerve fibers;
 Lymphatics;
 Remnants of the processus vaginalis
The fascias enclosing the contents of the spermatic cord include:
 The internal spermatic fascia, which is the deepest layer, arises from the transversalis fascia, and is attached
to the margins of the deep inguinal ring.
 The cremasteric fascia with the associated cremasteric muscle, which is the middle fascial layer and arises
from the internal oblique muscle;
 The external spermatic fascia, which is the most superficial covering of the spermatic cord, arises from the
aponeurosis of the external oblique muscle, and is attached to the margins of the superficial inguinal ring
Round ligament of the uterus

The round ligament of the uterus is a cord-like structure that passes from the uterus to the deep inguinal ring where
it enters the inguinal canal. It passes down the inguinal canal and exits through the superficial inguinal ring. At this
point, it has changed from a cord-like structure to a few strands of tissue, which attach to the connective tissue
associated with the labia majora. As it traverses the inguinal canal, it acquires the same coverings as the spermatic
cord in men.
Mechanics of the Inguinal Canal
The inguinal canal in the lower part of the anterior abdominal wall is a site of potential weakness in both sexes.
However the design of this canal attempts to lessen this weakness.
1. Except in the newborn infant, the canal is an oblique passage with the weakest areas,
namely, the superficial and deep rings, lying some distance apart. When the intra-abdominal
pressure rises, the anterior and posterior walls of the canal are approximated, thus
obliterating the passage. This is known as flap-valve effect.
2. The anterior wall of the canal (deep inguinal ring) is reinforced by the fibers of the internal oblique muscle
immediately in front of the deep ring.
3. The posterior wall of the canal (superficial inguinal ring) is reinforced by the strong conjoint tendon immediately
behind the superficial ring.
4. On coughing and straining, as in micturition, defecation, and parturition, the arching lowest fibers of the internal
oblique and transversus abdominis muscles contract, flattening out the arched roof so that it is lowered toward the
floor. The roof may actually compress the contents of the canal against the floor so that the canal is virtually closed
(Shutter Mechanism of the internal oblique)
5. Contraction of the Cremasteric muscle helps the spermatic cord to plug the superficial inguinal ring (Ball Valve
mechanism)
6. Contraction of the external oblique results in approximation of the two crura of the Superficial Inguinal Ring (Slit
Valve mechanism). The integrity of the superficial inguinal ring is greatly increased by the intercrural fibres.
7.Hormones may play a role in maintaining the tone of the inguinal musculature.
Development
Inguinal Canal represents the passage of Gubernaculum through the abdominal wall; it extends from the caudal end
of the developing gonad(in lumbar region) to the labioscrotal swelling. In early life, the canal is very short. As the
pelvis increases in width, the deep inguinal ring is shifted laterally and the adult dimensions are attained.
Clinical Aspects
1. Inguinal Hernia
An inguinal hernia is the protrusion or passage of a peritoneal sac, with or without abdominal contents, through a
weakened part of the abdominal wall in the groin. It occurs because the peritoneal sac enters the inguinal canal
either:
 Indirectly, through the deep inguinal ring (Indirect Inguinal Hernia);

 Directly, through the posterior wall of the inguinal canal (Direct Inguinal Hernia)
The indirect inguinal hernia is the most common of the two types of inguinal hernia and is much more common in
men than in women. It occurs because some part, or all, of the embryonic processus vaginalis remains open or
patent. It is therefore referred to as being congenital in origin.
A peritoneal sac that enters the medial end of the inguinal canal directly through a weakened posterior wall is a
direct inguinal hernia. It is usually described as acquired because it develops when abdominal musculature has been
weakened, and is commonly seen in mature men. The bulging occurs medial to the inferior epigastric vessels in the
inguinal triangle (Hesselbach's triangle), which is bounded:
 Laterally by the inferior epigastric artery;

 Medially by the rectus abdominis muscle;
 Inferiorly by the inguinal ligament
2.Vasectomy
Bilateral Vasectomy is performed to produce infertility. Under local anaesthesia, a small incision is made in the
scrotal wall and the vas deferens is divided between ligatures.
3.Cremasteric Reflex
Cremasteric Reflex is elicited by gentle touch at and around the skin of the medial aspect of the superior part of the
thigh. The sensory fibres enter the spinal cord at L1 level. Therefore it can be used to test spinal cord function at L1
level.
Spermatic Cord
The spermatic cord is a collection of structures that pass through the inguinal canal to and from the testis.
It begins at the deep inguinal ring lateral to the inferior epigastric artery and ends at the testis.
The Spermatic Cord consists of:
1- Vas deferens.
2- Artery of the vas.
3- Testicular artery.
4- Cremastric artery.
5- Testicular veins (pampiniform plexus).
6- Testicular lymph vessels.
7- Genital branch of the genitofemoral nerve, which supplies the cremaster muscle.
8- Autonomic nerves around the arteries.
9- Remains of the processus vaginalis.

Coverings of the Spermatic Cord (the Spermatic Fasciae)
The coverings of the spermatic cord are three concentric layers of fascia derived from the layers of the anterior
abdominal wall.
Each covering is acquired as the processus vaginalis descends into the scrotum through the layers of the abdominal
wall.
1- External spermatic fascia:
It is derived from the external oblique aponeurosis.
It is attached to the margins of the superficial inguinal ring.
2- Cremasteric muscle and fascia:
It is derived from the internal oblique muscle.
It is continuous with the lower arching fibers of the internal oblique.
3- Internal spermatic fascia:
It is derived from the fascia transversalis.
It is attached to the margins of the deep inguinal ring.
Scrotum
The scrotum is an out-pouching of the lower part of the anterior abdominal wall.
It contains the testes, the epididymides, and the lower ends of the spermatic cords.
The wall of the scrotum has the following layers:
1- Skin:
The skin of the scrotum is thin, wrinkled, and pigmented and forms a single pouch.
A slightly raised ridge in the midline indicates the line of fusion of the two lateral labioscrotal swellings.
In the female, the swellings remain separate and form the labia majora.
2- Superficial fascia:
This is continuous with the fatty and membranous layers of the anterior abdominal wall.
The fat is, however, replaced by smooth muscle called the dartos muscle.
This is innervated by sympathetic nerve fibers and is responsible for the wrinkling of the overlying skin.
The membranous layer of the superficial fascia (often referred to as Colles' fascia) is continuous in front with the
membranous layer of the anterior abdominal wall (Scarpa's fascia), and behind it is attached to the perineal body
and the posterior edge of the perineal membrane.
At the sides it is attached to the ischiopubic rami.
Both layers of superficial fascia contribute to a median partition that crosses the scrotum and separates the testes
from each other.
3- The external spermatic fascia is derived from the aponeurosis of the external oblique muscle.
4- The cremasteric fascia is derived from the internal oblique muscle.
5- The internal spermatic fascia is derived from the fascia transversalis.
The cremaster muscle is supplied by the genital branch of the genitofemoral nerve.
The cremaster muscle can be made to contract by stroking the skin on the medial aspect of the thigh.
This is called the cremasteric reflex.
The afferent fibers of this reflex arc travel in the femoral branch of the genitofemoral nerve.
The efferent motor nerve fibers travel in the genital branch of the genitofemoral nerve.
The function of the cremaster muscle is to raise the testis and the scrotum upward for warmth and for protection
against injury.
6- Tunica vaginalis:
It lies within the spermatic fasciae.
It covers the anterior, medial, and lateral surfaces of each testis.
It is the lower expanded part of the processus vaginalis; normally, just before birth, it becomes shut off from the
upper part of the processus and the peritoneal cavity.
The tunica vaginalis is thus a closed sac, invaginated from behind by the testis.
It consists of 2 layers:
1- Parietal layer: lines the internal spermatic fascia.
2- Visceral layer: covers the testis.
Lymph Drainage of the Scrotum
Lymph from the skin and fascia, including the tunica vaginalis, drains into the superficial inguinal lymph nodes
Child-Pugh Classification of Severity of Liver Disease
Modified Child-Pugh classification of severity of liver disease according to the degree of ascites, the plasma
concentrations of bilirrubin and albumin, the prothrombin time, and the degree of encephalopathy.
Parameter Points assigned

1 2 3
Ascites Absent Slight Moderate
Bilirrubin, mg/dL </= 2 2-3 >3
Albumin, g/dL >3.5 2.8-3.5 <2.8
Prothrombin time
* Seconds over control 1-3 4-6 >6
* INR <1.8 1.8-2.3 >2.3
Encephalopathy None Grade 1-2 Grade 3-4
A total score of 5-6 is considered grade A (well-compensated disease); 7-9 is grade B (significant functional
compromise); and 10-15 is grade C (descompensated disease). These grades correlate with one- and two-
year patient survival.
Grade Points One-year patient Two-year patient

survival (%) survival (%)
A: well- 5-6 100 85
compensated disease
B: significant 7-9 80 60
functional
compromise
C: descompensated 10-15 45 35
disease
Severity Criteria for Acute Pancreatitis
Ranson Criteria to Predict Severity of Acute Pancreatitis
1. When three or more of the following are present on admission, a severe course complicated by pancreatic
necrosis can be predicted with a sensitivity of 60-80%:
 Age over 55 years.
 White blood cell count over 16,000/uL.
 Blood glucose over 200 mg/dL.
 Serum lactate dehydrogenase (LDH) over 350 units/L.
 Aspartate aminotransferase (AST, SGOT) over 250 units/L.
2. Development of the following in the first 48 hours indicates a worsening prognosis:
 Hematocrit drop of more than ten percentage points.
 Blood urea nitrogen (BUN) rise greater than 5 mg/dL.
 Arterial PO2 of less than 60 mm Hg.
 Serum calcium of less than 8 mg/dL.
 Base deficit over 4 meq/L.
 Estimated fluid sequestration of more than 6 L.
3. Mortality rates correlate with the number of criteria present:
Number of criteria Mortality rate
0-2 1%
3-4 16%
5-6 40%
7-8 100%
Balthazar CT severity index for acute pancreatitis.
CT Grade Points Necrosis Additional Severity Mortality

(%) Points Index Rate (%)
A Normal pancreas 0 0 0 0 0
B Pancreatic 1 0 0 1 0
enlargement
C Pancreatic 2 < 30 2 4 0
inflammation and/or
peripancreatic fat
D Single 3 30-50 4 7 > 17
peripancreatic fluid
collection
E Two or more fluid 4 > 50 6 10
collections or
retroperitoneal air
Surgery Keynotes:
Causes of scaphoid abdomen:
1. Normal in thin patient.

2. Malnutrition.
3. Diaphragmatic hernia.
Causes of Discharge from the umbilicus: either bloody, serous, feces, urine or mucoid
1. Omphalitis : inflammation of the umbilicus causing serous or mucoid.

2. Vitleo-intestinal duct or Vitelline duct or omphalomesenteric duct (VID) this leads to leakage of feces.
3. Patent median umbilical artery which should be closed to form ligament (Urachus) this leads to leakage of
urine.
Urachus:
The urachus is a fibrous remnant of the allantois, a canal that drains the urinary bladder of the fetus that joins and
runs within the umbilical cord.
Failure for the lumen of the urachus to be filled in leaves a patent (open) urachus. The telltale sign is leakage of urine
through the umbilicus. A patent urachus needs to be surgically removed. There are four common pathology:
-Urachal cyst: there is no connection between the bladder and the umbilicus
-Urachal fistula: there is free communication between the bladder and umbilicus
-Urachal diverticulum (Vesicourachal diverticulum): the bladder exhibits outpouching
-Urachal sinus: the pouch opens toward the umbilicus
-Normal Intestinal peristalsis: 4-6/ min.
-Most common cause of death in SCA patients are:
1. Acute chest syndrome.

2. Sequestration in the liver or spleen.
3. Stroke & Transient Ischemic Attack
4. Acute coronary syndrome.
-Jaudice appears firstly in the sclera due to rich connective tissue elastin which is hydrophilic to bilirubin,
clinicaly early seen prominent by nein light.
Complications of thyroidectomy:
• Wound infection
• Anaesthetic complications
• Haemorrhage
• Hypoparathyroidism
• Recurrent laryngeal nerve injury
• Damage to surrounding structures – oesophagus/trachea/laryngeal muscles
• Thyrotoxic crisis
• Tracheal obstruction (Laryngeal oedema)
Common Abdominal Signs and Findings Noted on Physical Examination
Sign or Finding Description Associated Clinical Condition(s)

Aaron sign Referred pain or feeling of distress in epigastrium or precordial region on Acute appendicitis
continued firm pressure over the McBurney point
Ballance sign Presence of dull percussion note in both flanks, constant on left side but Ruptured spleen
shifting with change of position on right side
Bassler sign Sharp pain elicited by pinching appendix between thumb of examiner and Chronic appendicitis
iliacus muscle
Beevor sign Upward movement of umbilicus Paralysis of lower portions of rectus
abdominis muscles
Blumberg sign Transient abdominal wall rebound tenderness Peritoneal inflammation
Carnett sign Disappearance of abdominal tenderness when anterior abdominal muscles Abdominal pain of intra-abdominal origin
are contracted
Chandelier sign Intense lower abdominal and pelvic pain on manipulation of cervix Pelvic inflammatory disease
Charcot sign Intermittent right upper quadrant abdominal pain, jaundice, and fever Choledocholithiasis
Chaussier sign Severe epigastric pain in gravid female Prodrome of eclampsia
Claybrook sign Transmission of breath and heart sounds through abdominal wall Ruptured abdominal viscus
Courvoisier sign Palpable, nontender gallbladder in presence of clinical jaundice Periampullary neoplasm
Cruveilhier sign Varicose veins radiating from umbilicus (caput medusae) Portal hypertension
Cullen sign Periumbilical darkening of skin from blood Hemoperitoneum (especially in ruptured
ectopic pregnancy)
Cultaneous Increased abdominal wall sensation to light touch Parietal peritoneal inflammation secondary
hyperesthesia to inflammatory intra-abdominal
pathology
Dance sign Slight retraction in area of right iliac fossa Intussusception
Danforth sign Shoulder pain on inspiration Hemoperitoneum (especially in ruptured
ectopic pregnancy)
Direct abdominal â€‖ Localized inflammation of abdominal
wall tenderness wall, peritoneum, or an intra-abdominal
viscus
Fothergill sign Abdominal wall mass that does not cross midline and remains palpable Rectus muscle hematoma
when rectus muscle is tense
Grey Turner sign Local areas of discoloration around umbilicus and flanks Acute hemorrhagic pancreatitis
Iliopsoas sign Elevation and extension of leg against pressure of examiner's hand causes Appendicitis (retrocecal) or an
pain inflammatory mass in contact with psoas
Kehr sign Left shoulder pain when patient is supine or in the Trendelenburg position Hemoperitoneum (especially ruptured
(pain may occur spontaneously or after application of pressure to left spleen)
subcostal region)
Kustner sign Palpable mass anterior to uterus Dermoid cyst to ovary
Mannkopf sign Acceleration of pulse when a painful point is pressed on by examiner Absent in factitious abdominal pain
McClintock sign Heart rate > 100 beats/min 1 hr post partum Postpartum hemorrhage
Murphy sign Palpation of right upper abdominal quadrant during deep inspiration Acute cholecystitis
results in right upper quadrant abdominal pain
Obturator sign Flexion of right thigh at right angles to trunk and external rotation of same Appendicitis (pelvic appendix); pelvic
leg in supine position result in hypogastric pain abscess; an inflammatory mass in contact
with muscle
Puddle sign Alteration in intensity of transmitted sound in intra-abdominal cavity Free peritoneal fluid
secondary to percussion when patient is positioned on all fours and
stethoscope is gradually moved toward flank opposite percussion
Ransohoff sign Yellow pigmentation in umbilical region Ruptured common bile duct
Rovsing sign Pain referred to the McBurney point on application of pressure to Acute appendicitis
descending colon
Subcutaneous Palpable crepitus in abdominal wall Subcutaneous emphysema or gas gangrene
crepitance
Summer sign Increased abdominal muscle tone on exceedingly gentle palpation of right Early appendicitis; nephrolithiasis;
or left iliac fossa ureterolithiasis; ovarian torsion
Ten Horn sign Pain caused by gentle traction on right spermatic cord Acute appendicitis
Toma sign Right-sided tympany and left-sided dullness in supine position as a result Inflammatory ascites
of peritoneal inflammation and subsequent mesenteric contraction of
intestine to right side of abdominal cavity
Charcot's triad :
 biliary colic
 Intermittent jaundice
 swinging pyrexia - fever and chills
Courvoisier's law:
Courvoisier's law states that, in the presence of jaundice, an enlarged gallbladder is unlikely to be due to gallstones;
rather carcinoma of the pancreas or the lower biliary tree is more likely.
Table: 61.2 Child's Classification of hepatocellular function

Group designation A B C
Bilirubin mg/dl < 2.0 2.0-3.0 >3.0
Albumin g/dl >3.5 3.0-3.5 <3.0
Ascites None Easily controlled Poorly controlled
Neurological None Minimal Advanced
disorder
Nutrition Excellent Good Wasting
Reference : Bailey & Love's Short Practice of Surgery 25th ED CH: 61. The Liver page
1083
SURGICAL SKILLS
BREIF REVIEW ABOUT SURGICAL SKILLS TAUGHT
COLLEGE OF MEDICINE
IN AL-AHSSA

Group : B3
AC:207002113
CONTENTs
-Examination of Ulcers.
-Examination of Thyroid.
-History taking, patient interview, & communication.
-Examination of Swellings.
-Examination of Breast.
-Examination of inguinal hernia.
-Examination of Abdomen.
-NGT, Urinary Catheter, & IV canula.
-Management of trauma patient.
-Examination of a Diabetic foot.

SURGICAL SKILLS
1-Examination of ulcers Date: 24-05-2010
Inspection:
Site.
Color of the surrounding skin.
Size in three direction in cm.
Depth of the ulcer
Shape as (circular, oval, or irregular)
Temperature & tenderness.
Edges
Margin
Floor (Color, Granulation, Pinkish, Yellowish)
Discharge (Slough, Puss, Forthy discharge, Turbid, Serous, Sanguinous, or purulent).
Palpation:
Size.
Edges (slopping, punched out, undermined, rolled, or everted).
Margin.
Base.
Draining lymph node (Axillary, or inguinal).
Others:
General Examination.
Neurological Examination.
Respiratory exam.
Cardiovascular exam.
2-Examination of Thyroid: Date: 26-05-2010
General look to the patient for signs of nervousness, agitation, irritability, generalized
weight loss, muscle wasting,.
Eye for signs of:

Exophthalmos (forward push of the eye) due to increased retro-orbital fat & connective
tissue deposition & edema , look for difficulty in convergence , lid lag, lid retraction , look
upward without wrinkling the forehead.
Look for chemosis (Edema of the conjunctiva) due to obstruction of the lymphatic &
venous drainage of the conjunctiva by the increased retro-orbital pressure.
Look for Ophthalmoplegia (Weakness of the ocular muscles) due to cellular infiltration of
the muscles & oculomotor nerve supplying them affecting mainly superior, & lateral recti, &
inferior oblique muscle which prevent the patient from looking upward & outward.
Look to the Hand: tremors, sweating, pulse.
Inspection:
Base of the tongue.
Movement of the neck swelling with swallowing.
With tongue protrusion.
Palpation:
The thyroid (in front and behind , and with swallowing).
Palpation of the lower border of the thyroid if palpable.
Palpation of the trachea, cervical lymph nodes and sternocleidomastoid.
Percussion: of manubrium sterni.
Auscultation: carotids and thyroid for bruit.
3-History taking, Patient communication & Interview: Date: 31-05-2010

Date / / On ……………
Personal Data:
• Name
• Age
• Sex
• MS
• Occupation
• Residency
• Nationality
• Religion
• Admitted through ( ER or OPD ) on ( Saturday or ………. )
Chief complains ( in patient’s words ):

• The problem ( pain , lump, ulcer, vomiting , …………)
• +
• Duration
History of present illness (in doctor’s words).
Past History:
• previous attacks of the same problem
• previous operation of the same problem or different problem
• history of DM, hypertension, sickle cell anemia, asthma
• blood transfusion
• any food allergy
Family History:
• Previous attacks of same problem (if yes, did operation?)
• History of DM, hypertension, sickle cell anemia, asthma (Father, mother).
Drug History:
• Any specific drug
• Any drug allergy
Social History & Habits:

• Smoker?
• Traveling
• Exercise
• Diet (mainly, increased in what? Or decreased in what )
-Developing communication skills is one of the important skills that most of the doctors are
deficient.
-Getting trust of the patient is an important step in both history taking & examination but
more in history.
-Interview of the patient should be on trust that the doctor knows the questions to ask.
4-Examination of Swelling Date: 2-06-2010

History:
When did you notice it?
How did you notice it?
Did you have a similar swelling in the past?
Have you had any other swelling in the body?
Have this swelling increased in size?or vanish? When did it reappear?
Examination:
Inspection: site, size, shape, surface, solitary or multiple, overlying and surrounding skin,
color, local movement of the swelling, pulsation , compression effect, cough impulse.
Palpation: temperature, tenderness, confirm size, & shape of the swelling, surface,
consistency, edge pertaining to lymph node.
If the swelling is soft test: fluctuation, fluid thrill, transillumination, cough impulse,
compressibility, & reducibility.
Fixity to the skin, underlying structures, pulsatility.
Percussion for big swelling to suspect the content of the swelling as gas, fluids, hard
structures.
Auscultation: for bruit.
Focal examination: lymph nodes, compression effect, joints near to the swelling, test for
metastasis if suspected.
5-Examination of Breast Date: 07-06-2010 Monday
History: Age, Previous pregnancies, menstrual history, Drug history, Family history,
lactation & breast feading.
CC: Lump , Pain, Discharge, or Redness, in the breast.
Inspection: contours, size, symmetry, direction of nipples and for movement of the breasts
with changing in posture, look for dimpling of the breast. Look for the axilla, arms, &
supraclavicular fossa for any visible masses.
Palpation: for glandular tissue and lumps and axillary lymph nodes, movement in
longitudinal or horizontal lines or clockwise palpation.
6-Examination of an inguinal swelling Date:09-06-2010Wednesday

Inspection:
-Site.
-Size.
-Shape.
-Surface.
- Overlying and surrounding skin.
-Any visible pulsation and for cough impulse.
Palpation:
-Tempreture.
-Tenderness
-consistency
-Edges pertaining to lymph node
-Tranillumination
- Reducibility,& compressibility
- Palpation of superficial inguinal ring, testes, epididumis, spermatic cord and the vas
deferens.
Inguinoscrotal vs. scrotal swellings (inspection):
o Is the upper margin of the swelling confined to the scrotum?
o Determine relation to pubic tubercle
o Upper and medial: inguinal hernia.
o Lower and lateral: femoral hernia.
o Is there a visible or palpable Cough impulse?
o The presence of an expansile cough impulse is diagnostic hernia but its absence does not
exclude hernia.
o Is the swelling reducible on lying down?
o Does it reappear on standing and coughing?
o Are there any inguinal or abdominal scars?
Tests for hernia:

External ring invagination test:
• Patient lying down/erect position
• Reduce the hernia gently
• Invaginate your little/index finger through base of scrotum into external ring
• Ask the patient to cough
• Feel the impulse
Impulse stick above finger is direct hernia.
Impulse stick tip finger is indirect hernia.
• Assess the strength of posterior wall
Internal ring occlusion test:

 Patient lying down
 Reduce hernia gently
 Mark the internal ring and occlude with thumb
Put thumb on anterior superior iliac supine and middle finger in pubic sympesis at the same time put
other thumb above 1.25 cm from the previous hand.
 Ask the patient to cough
 Look for reappearance of swelling
Reappearance of swelling is direct hernia.
Absent swelling is indirect hernia.
Examination of the spermatic cord

• Look for increase in size and any signs of inflammation
• Does it have a feeling of ―bag of worms‖?
• cough impulse?
• Does it reduce on lying down?
• Is the vas deferens smooth or beaded?
External Genitalia
• Position and size of external meatus; any pus discharge
• Bending of the penis: Chordee
• Phimosis or paraphimosis in uncircumcised
• Ulcers on the glans or the shaft of penis
• Floor of the urethra for strictures
7-Examination of the abdomen Date:14-06-2010 Monday

-Inspection:
contours of the abdomen, site of the umbilicus, any masses, ulcerswith discharge, and for
scars, stretch marks, pigmentation and movement with respiration.
-Palpation:
First palpate for tempreture & tenderness, perform superficial & deep palpation palpate for
any visible masses from the liver, spleen, & kidneys.
-Percussion:
Liver span, spleen, fluid thrill and shifting dullness
-Auscultation:
for peristalsis and for bruits.
-Examination of the groin region.
-Per rectal & or per vaginal examination.
8-NGT, Urinary Catheter, & IV canula Date:16-06-2010Wednesday
-I V cannula:
Localized site of injection in a strait vein from distal to proximal and technique of applying
it, proper size cannula (Every thing is written in the bag of the cannula) and choose a patent
vein and differentiate it from thrombosed vein (Patent vein is usually elastic fluctuant while
thrombosed vein is solid or firm).
-NGT:
1- Choose the appropriate patent nostril and lubricate the tube.
2- Measure the length of the tube.
3- Passes the tube into the stomach, with anatomical consideration of the course.
4- Confirm that the tube is in the stomach.
5- Ability to aspirate gastric juice.
Notes:
-NGT containing Blue line (Lead) along its length responsible radio-opaque density in x-ray
film.
-NGT length is 1.25 meter.
-Consider NGT for pediatrican.
-Do not miss to advice the patient to drink something while inserting the tube along the
oropharenx & the esophagus to prevent it from passing to the trachea.
-Urinary catheter:
1- Differentiate between different catheter types (Urinary catheter, Foley’s catheter).
2- Identify different types of foley's catheter.
3- Prepare the parts and drapes the area.
4- Passes the catheter successfully (After lubrication), considering variation in each sex.
5- Inflate the catheter ballon with saline to maintain its position.
6- Connects the catheter to a collection bag and straps the catheter properly.
Notes:
-Consider the difference between foley’s catheter (with ballon)& normal urinary catheter
(without ballon).
-Consider the contraindications of urinary catheter & the alternative as (Suprapubic
cystostomy, & Nephrostomy) as pelvic fractures as after trauma in the pelvis, & injury in the
urethra.
-Consider different types of catheter as rubbery, or silicon catheter.
9-Management of Trauma patient Date: 21-06-2010 Monday

Management of the traumatic patient:
 Pre-hospital phase.
 Primary Assessment.
 Secondary Assessment.
-Casuality sorting (Triage):
Sorting of the patients according to the grade and severity of the injuries.
- Team working & cooperation.
Priorites for sorting:
-Stage 1 = Resuscitation and immediate surgery.
-Stage 2 = No surgery(minor trauma&those with very bad injury and very low chance of
survival).
-Stage 3 = wait for surgery(majority of patients with head or extremities injury).
 Pre-hospital phase: ABC
1. Airway – Cervical spine.
2. Breathing.
3. Circulation
4. Control of bleeding
5. Immobilization
6. IV line.
7. Immediate appropriate transfer to the nearest Emergency unit.
Primary assessment: ABCDE

 Air way obstruction + C-spine stabilization.
 Breathing problems: Tension Pneumothorax, Open Pneumothorax.
 Circulation: Shock, Cardiac tamponade, Hemorrhage.
 Disabilities: AVPU, Pupils
 Exposure / Environmental control
Added tools used:
 ECG monitoring.
 Urinary and Gastric Catheters.
 Monitoring: RR, ABG, Pulse Oximetry, ABP, PR, Urine O/P, Temp .,CVP / JV.
 X-ray and diagnostic: CXR, Pelvis, Lateral. C-spine and Diagnostic peritonel Lavage and abdominal
ultra sound. As indicated
Resuscitation: Restoring organ perfusion.
Secondary assessment:
 Complete History.
 Head to toe examination including the organ systems.
 Re-assessment of vital signs.
 Complete neurological examination GCS.
 Special procedures, Specific X-rays and laboratory studied.
Definitive care: According to the clinical and other data the patient will be taken to OR, ICU or others.
Transfer: To other facility according to the patient need and our capability.
10-Examination of a Diabetic Foot Date: 23-06-2010 Wednesday
Diabetic foot:
It is defined as the foot of diabetic patients with ulceration, infection and / or destruction of the deep tissues,
associated with neurological abnormalities and various degrees of peripheral vascular disease in the lower
limb
Aetiology of diabetic foot:

 Neuroischemic
 Ischemic ―rare‖
 Hyperglycemias
 Trauma
History:
 Age/sex
 Mode of onset
 Pain in limb
o Onset
o Site of pain ?
o Aggravating/relieving factors
o ―intermittent claudication‖ CRAMPY
o Rest pain
 Systemic angiopathy
 Personal history- smoking
 Family history- diabetes
Clinical presentation in diabetic foot:

 Pain
 Infection
 Skin changes of ischemia
 Deformities
 charcot’s joint
Assessment:
 Neuropathic assessment:
 Sensory
o Fine touch
 Motor
o Bulk/wasting
o Power
o Deformities
 Autonomic
o Dryness
o Color change
 Vascular assessment:
 Skin temp.
 Capillary filling time
 The ankle brachial pressure index (ABPI)
 s/s of chronic ischemia:
o  hair growth/ Loss of hair
o Thin shiny skin
o Loss of SC fat
o Oedema
o Trophic changes in nails
o  pain on elevation of limb
o Ulceration
o Dusky colour
 Retinopathy
 Nephropathy
Palpation of blood vessels:
• Arteries:
o Dorsalis pedis
o Posterior tibial
o Popliteal
o Femoral
o Radial
o Brachial
o Sub clavian
o Common carotid
SURGERY I ASSIGNMENT
ACUTE LIMB ISCHEMIA
2010- second semester
Edited by: Qasim Hussain Al-Haleimi
4th Year medical student
AC: 207002113
SUPERVISIED BY:
Dr. Mohammad Atif Khan.
CONTENTS:
-Learning objectives.
-Blood supply of the lower Limb.
-Epidemiology.
-Causes
- Pathogenesis.
-Clinical Features (History & Examination).
-Claudication.
-Manifestation of claudication.
-Classification & stages.
-Investigations.
-Treatments & Interventions.
Complications of the interventions.
-Conclusion
-References.
Learning Objectives:
-Blood supply of the lower limb.
-Definition & classes of ALI.
-Pathophysiology of ALI.
-Embolism vs Thrombosis.
-Clinical Presentation.
-History.
-Claudication.
-Physical Examination.
-Investigation.
-Management.
-Complications.
ACUTE LIMB ISCHEMIA
Blood supply of the lower limb:
A) THE THIGH:
1) Femoral Artery:
-Origin: the abdominal aorta terminates at the level of fourth lumbar vertebra by dividing into: Right and
Left common iliac arteries. Each one of these arteries will divide into internal and external iliac arteries. The
external iliac artery will continue as Femoral artery behind the inguinal ligament, midway between the
anterior superior iliac spine and the pubis symphysis.
-Course: Then it descends downward and medially from the base to the apex of the femoral triangle. From
the apex of the femoral triangle, the artery will descends vertically downward through the adductor canal.
-Relations: the artery is covered by skin, superfacial and deep facia, and it is superfacial to the psoas major
muscle, pectineus and adductor longus muscles. It is in the middle between the femoral vein medially and
the femoral nerve laterally.
-Branches: the artery gives the following branches:
a) Superfacial inguinal arteries:
1- Superfacial external pudendal artery
2- Superfacial epigastric artery
3- Superfacial circumflex iliac artery
b) Profunda femoris artery
c) Deep external pudendal artery
d) Descending genicular artery
2) Femoral Vein:
-Origin: it is the continuation of the popliteal vein at the opening of the adductor magnus muscle.
-Termination: it is terminate by continuation as external iliac vein.
-Tributaries: Great saphenous vein, Profunda femoris vein, Medial circumflex femoral vein and deep
external pudendal vein.
B) THE GLUTEAL REGION:

1) Superior Gluteal Artery:
-Origin: it is branch from the internal iliac artery. It enters the gluteal region by passing through the greater
sciatic foramen.
-Branches: It gives branches to the surrounding structures of the upper part of the gluteal region.
2) Inferior Gluteal Artery:

-Origin: it is branch from the internal iliac artery. It enters the gluteal region by passing through the sciatic
foramen.
-Branches: it gives branches to the surrounding structures of the lower part of the gluteal region.
3) Internal Pudendal Artery:

-Origin: it is branch from the internal iliac artery. It enters the gluteal region by passing through the greater
and lesser sciatic foramen.
-Branches: Inferior rectal artery, scrotal artery, artery of the bulb, Dorsal artery of the penis and Deep artery
of the penis.
C) POPLITEAL REGION:
1) Popliteal Artery:
-Origin: it is continuation of the femoral artery at the opening of the adductor magnus muscle.
-Relations: it is covered by the skin, fasciae, tibial nerve and popliteal vein. It is superfascial to the popliteus
muscle and femurs bone.
-Termination: it terminates at the lower border of the popliteus muscle by dividing into: Anterior tibial artery
and Posterior tibial artery.
-Branches: it gives branches to the surrounding structures.
2) Popliteal Vein:
-Origin: it is formed by the union of the anterior and posterior tibial veins.
-Termination: it ends at the opening of the adductor magnus muscle by continuation as femoral vein.
-Tributaries: Small saphenous vein and many ones from the surrounding structures.
D) THE LEGS:
1) Anterior tibial artery:
-Origin: it is the smaller of the tow terminal branches of the popliteal artery, at the lower border of the
popliteus muscle.
-Relations: it enters the anterior compartment of the leg by passing through the opening in the interosseous
membrane in relation to the deep peroneal nerve. In the lower part of the anterior side of the leg, it lies
superfacial and its pulsation can be felt.
-Termination: it terminates in front the ankle joint, midway between the tow malleoli, by continuation as
dorsalis pedis artery at the dorsum of the foot.
-Branches:
1- Anastomotic branches with the anterior and posterior tibial recurrent artery.
2- Multiple branches to the muscle of the anterior compartment of the leg.
2) Posterior Tibial Artery:

-Origin: it is the larger of the tow terminal branches of the popliteal artery.
-Course: it descends in the posterior compartment of the leg in relation to the tibial nerve.
-Termination: it terminates midway between the medial malleolus and the medial tubercle of the calcaneus
by dividing into: Medial planter artery and Lateral planter artery.
-Branches:
1- Peroneal artery
2- Muscular branches to the muscles of the posterior compartment of the leg.
3- Nutrient branch to the tibia
4- Anastomotic branches
E) THE FOOT:
1) Medial Planter Artery:
-Origin: it one of the tow terminal branches of the posterior tibial artery.
-Course: it enters the sole of the foot by passing deep to the abductor hallucis muscle, and then it passes
forward medial to the medial planter nerve and terminates at the base of the first metatarsal bone by
supplying the medial side of the big toe.
2) Lateral Planter Artery:

-Origin: it is the larger of the tow terminal branches of the posterior tibial artery, midway between the
medial malleolus and the medial tubercle of the calcaneus.
-Course: it enters the sole of the foot deep to the abductor hallucis muscle, lateral to the lateral planter nerve.
It ends by anastomosing with the dorsalis pedis artery at the proximal end of the first interosseous space the
forms the planter arch.
3) Dorsalis Pedis Artery:

-Origin: it is continuation of the anterior tibial artery in front of the ankle joint.
-Course: it passes medial to the deep peroneal nerve. It is just covered by skin and superfacial fascia so, its
pulsation can be felt on the dorsum of the foot.
-Termination: it ends at the sole of the foot by anastomosing with the lateral planter artery to forms the
planter arches.
-Branches:
1- Lateral and medial tarsal arteries.
2- Arcuate artery that supplies the second, third, fourth and fifth toes and the lateral side of the littile toe.
3- First dorsal metatarsal artery that supplies both sides of the big toe and the medial side of the second toe.
4- First planter metatarsal artery.
Definition:
Acute limb ischemia occurs when an arterial occlusion suddenly reduces blood flow to the arm or leg.
The metabolic needs of the tissue outstrip perfusion, placing limb viability in jeopardy.
Classification:
According to Society of Vascular Surgery/International Society of Cardiovascular Surgery (Rutherford et al, 1997) ALI
can be classified to 3 stages:
Findings Doppler Signals
Category Description/Prognosis Muscle
Sensory Loss Arterial Venous
Weakness
I. Viable Not immediately threatened None None Audible Audible
II. Threatened
a. Minimal (toes) or
Salvageable if promptly treated None Inaudible Audible
Marginally none
More than toes,
b. Salvageable with immediate
associated with rest Mild, moderate Inaudible Audible
Immediately revascularization
pain
Profound,
III. Major tissue loss or permanent Profound,
paralysis Inaudible Inaudible
Irreversible nerve damage inevitable anesthetic
(rigor)
Epidemiology:
No a lot data available but it is reported to occur by rate of 14 out of 100,000 per year in USA.The prevalence of
peripheral vascular disease in people aged over 55 years is 10%–25% and increases with age. In the USA peripheral
arterial disease affects 12–20 percent of Americans age 65 and older. Approximately 10 million Americans have PVD.
Despite its prevalence and cardiovascular risk implications, only 25 percent of PAD patients are undergoing treatment.
Risk Factors:
-Smoking
- Dyslipidemia
- DM
-Hypertension
CAUSES:
The most common causes are:
 Embolism (main causes):

o Left atrium in patients in atrial fibrillation.
o Mural thrombus after myocardial infarct.
o Prosthetic and diseases heart valves.
o Aneurysm or atheromatous stenosis.
o Outside compression of a blood vessel, e.g. by a tumor, foreign body, Paradoxical
embolism.
 Thrombosis (main causes):
o Hypercoagulability.
o Endothelial cell injury.
o Hemodynamic changes (stasis, turbulence).
o Left atrial appendage.
o Cancers or malignancies such as leukemia.
 Combination of the 1st two may produce the obstruction.
Less common causes are:
 Arterial stenosis.
 Atrial trauma.
 Dissecting aneurysm.
 Arteritis (e.g. Giant cell arteritis, Buerger's Thromboangiitis obliterans).
 Thrombophlebitis.
 Arterisal occlusion.
 Arteriosclerosis.
 Vasospasm with thrombosis (e.g. ergotism).
 Popliteal cyst with thrombosis.
 Popliteal entrapment with thrombosis.
 Spontenous thrombosis associated with a hypercoagulable state.
 Diabetes mellitus.
 Tachycardia.
 Hypertension.
 Sickle cell disease (abnormally shaped red blood cells).
 Induced g-forces which restrict the blood flow and force the blood to the extremities of the body, as
in acrobatics and military flying.
 Localized extreme cold, such as by frostbite, ice, or improper Cold compression therapy.
 Tourniquet application.
 An increased level of glutamate receptor stimulation.
 Congenital (e.g. arteriovenous malformations, arterial fibromuscular dysplasia syndrome).
 Raynaud's syndrome (Vasospastic disorder).
 Toxicity.
Pathogenesis:
1-Acute Embolic Ischemia:

- An embolus can originate from the heart (MS with atrial fibrillation, MI with mural thrombus) or
dilated diseased arteries (aortic aneurism).
-An embolus suddenly occludes a relatively healthy arterial tree.
-It usually arrest at arterial bifurcation (like Aortic bifurcation, Iliac bifurcation, Femoral bifurcation,
Popliteal trifurcation).
2- Acute Thrombotic Ischemia:

The pathophysiolgy of acute thrombotic ischemia can be explained by atherosclerosis pathogenesis,
which is:
The initial event in atherosclerosis is infiltration of low-density lipoproteins (LDLs) into the
subendothelial region. The endothelium is subject to shear stress, the tendency to be pulled along or
deformed by flowing blood. This is most marked at points where the arteries branch and this is where
the lipids accumulate to the greatest degree.
The LDLs are oxidized or altered in other ways. Thus, altered LDLs activate various components of
innate immune system including macrophages, natural antibodies, and innate effector proteins such as
C-reactive protein and complement. Altered LDLs are recognized by a family of scavenger receptors
expressed on macrophages. These scavenger receptors mediate uptake of the oxidized LDL into
macrophages and the formation of foam cells. The foam cells form fatty streaks. The streaks appear in
the aorta in the first decade of life, in the coronary arteries in the second decade, and in the cerebral
arteries in the third and fourth decades
Oxidized LDLs have a number of deleterious effects, including stimulation of release of cytokines and
inhibition of NO production. Vascular smooth muscle cells in the vicinity of foam cells are stimulated
and move from the media to the intima, where they proliferate, lay down collagen and other matrix
molecules, and contribute to the bulk of the lesion. Smooth muscle cells also take up oxidized LDL and
become foam cells. Lipids accumulate both intracellularly and extracellularly.
As the atherosclerotic lesions age, T cells of the immune system as well as macrophages are attracted
to them. The intercellular "soup" in the plaques contains a variety of cell-damaging substances,
including ozone. Overall, the lesions have been shown to have many of the characteristics of a low-
grade infection. Growth factors and cytokines involved in cell migration and proliferation are also
produced by smooth muscle cells and endothelial cells, and there is evidence for shear stress response
elements in the flanking DNA of relevant genes in the endothelial cells. A number of investigators have
searched for bacteria in plaques, and in a significant number Chlamydophila pneumoniae—an organism
usually associated with respiratory infection—has been found. However, other organisms have also
been found, and it is too early to say whether the chlamydiae are causative agents or merely
coincidental tenants in the lesions.
As plaques mature, a fibrous cap forms over them. The plaques with defective or broken caps are most
prone to rupture. The lesions alone may distort vessels to the point that they are occluded, but it is
usually rupture or ulceration of plaques that triggers thrombosis, blocking blood flow.
A characteristic of atherosclerosis that is currently receiving considerable attention is its association

with deficient release of NO and defective vasodilation. As noted, oxidized LDLs inhibit NO production.
If acetylcholine is infused via catheter into normal coronary arteries, the vessels dilate; however, if it is
infused when atherosclerosis is present, the vessels constrict. This indicates that endothelial secretion
of NO is defective.
Embolism vs Thrombosis:
Difference Thrombosis Embolism
Definition A blood clot that forms in The obstruction of a blood

a blood vessel or in the vessel by a foreign substance
heart and does not move or a blood clot blocking the
to another area of the vessel. Something travels
through the bloodstream,
body.
lodges in a vessel and plugs
it.
Source No obvious cardiac source obvious cardiac source
Onset gradual blockage of the sudden and severe onset
artery
Causes Atherosclerosis Prolonged Immobilization
Pathogenesis Atherosclerosis causes Prolonged

progressive narrowing of Immobilization stasis of
the arterial tree blood thrombus
Stimulates development formation when the
of collaterals Sluggish patient move his or her
flow & rough surface will leg the thrombus
favor acute thrombosis. dislodged embolus
Clinical Features 1- History of claudication 1-No History of

claudication
2- Abnormal pulses in 2- Normal pulses in
both side contralateral limb
3- Few collateral
3-well developed
collateral
Investigation Angiogram: diffuse Angiogram: minimal
atherosclerotic atherosclerotic
common sites that usually involved in embolism occlusion are:
. The femoral artery bifurcation which account for (43%), followed by the iliac arteries (18%), the aorta
(15%), and the popliteal arteries (15%).
The site of occlusion, presence of collateral circulation, and nature of the occlusion (thrombus or embolus)
determine the severity of the acute manifestation. Emboli tend to carry higher morbidity because the
extremity has not had time to develop collateral circulation.
Clinical Features:
Patients with acute limb ischaemia can present with:
1- Intermittent claudication
2- Rest pain:
A continuous, unremitting pain caused by severe ischaemia. In contrast to intermittent
claudications, this pain present at rest throughout the day and the night.
3- Pre-gangrene:
The principal symptom of pre-gangrene is rest pain. The principal signs are pallor of the tissues
when elevated, congestion when dependent, guttering of the veins, thick and scaling skin, and
wasting of the pulps of the toes or fingers. The limb is cold with poor refilling.
4- Gangrene:
The nerves is the dead part die, therefore gangrenous tissues are not painful. The junction
between the normal and dead tissue gradually become distinct which is known as "line of
demarcation". The living tissue proximal to the line of demarcation is usually ischaemic and so often
constantly painful "rest pain" and tender.
The gangrene could be infected "wet" or non-infected "dry", and eventually it can lead to
ischaemic ulceration.
Leriche's syndrome
Also known as "Aortoiliac occlusive disease" is a disturbance usually affecting young males caused by
atheromatous involvement or occlusion of the abdominal aorta by a thrombus just above the site of its
bifurcation (obliteration of both A. iliacae communes). The characteristic symptoms include:
 Inability to maintain penile erection.

 Fatigue of both lower limbs.
 Intermittent bilateral claudications with ischemic pain.
 Absent or diminished femoral pulses along with pallor or coldness of both lower extremities.
Clinical differentiation between thrombosis & embolism:
Embolism Thrombosis
obvious cardiac source No obvious cardiac source
No History of I.cluadication history of I.cluadication
Normal pulses in contralateral limb abnormal pulses in both side
Angiogram: minimal atherosclerotic Angiogram: diffuse atherosclerotic
Few collateral Well developed collateral
History:
Presenting complaints:
Resting pain, which develops suddenly, in the limbs.
Past History:
The patient come with a history of:
-Claudication which is usually intermittent in character.
-Heart diseases as (atrial fibrillation).
-Aneurysms ( or possible embolic sources).
-DVT.
-Vasculitis.
-Atherosclerotic risk factors:
Hypertension, Diabetes, tobacco abuse, hyperlipidemia.
Family history :
heart attacks, strokes, blood clots, or amputations.
Symptoms & Signs:
-Claudication (fatigue+pain) from intermittent ischemia.
-Rest Pain – more severe ischemia; color changes – limb threatening; Treatment: aggressive
-Ischemic ulcers in the distal part of the extremities
Ischemic Ulcer
-Gangrene of the foot.
-Neurological manifestations as decrease in sensation numbness & tingling .
-Pallor.
-Paralysis.
-Parasthesia.
Examination:
Inspection & palpation:
5Ps:
Pallorness.
Pulselessness or unequal pulses.
Paresthsia.
Paralysis.
Pain.
Poikilothermy (Coldness).
Pigmentations.
Auscultation:
Bruits in aortic, iliac, femoral, or popliteal artery.
Ankle Brachial Index (ABI)= Lower extremity systolic pressure / Brachial artery systolic pressure
Normally should be 1 while in this disease ABI˂ 1.
Monitoring of ABI
Ankle Brachial Index (ABI)

 It is important to note that the ankle-brachial index ABI is measured only if arterial signals are found
on Doppler ultrasound.
 The ABI is derived from the ankle systolic pressure and the brachial systolic pressure and is
determined as follows. The systolic pressure is measured in each arm, and the higher of the two
measurements is taken to be the brachial systolic pressure. A cuff is then placed on each calf, and
the examiner listens to signals in the dorsalis pedis and posterior tibial arteries. The cuff is inflated
until the signal is no longer heard. At this point, the cuff is slowly released, and the systolic pressure
is recorded at the point where the signal is once again audible. Again, the higher of the two systolic
measurements is taken to be the ankle systolic pressure. The systolic ankle pressure is then divided
by the brachial systolic pressure to yield the ABI. An ABI in the range of 1 is normal. When the ABI
falls below 0.6, there is a significant difference in blood pressure between the proximal arterial tree
and the distal extremity, which usually denotes an occlusive process.
Claudication:
Intermittent claudication is defined as an aching pain in the leg muscles, usually the calf, which is precipitated by
walking and isrelieved by rest.
-Claudication pain is always reversible and relieved by rest.
- Claudication tends to improve with time and exercise due to the opening up of new collateral supply vessels and
improved muscle function.
- The site of disease is one level higher than the highest level of affected muscles.
- Most patients with claudication have associated vascular disease and investigation for occult coronary or
cerebrovascular is mandatory.
- Cauda equina ischaemia caused by osteoarthritis of the spine can also cause intermittent claudication.
Differential diagnosis
Vascular
Atheroma
• Typical patient: male, over 45 years, ischaemic heart disease, smoker, diabetic, overweight.
• Aortic occlusion: buttock, thigh and possibly calf claudication, impotence in males, absent femoral pulses and
below in both legs (Leriche’s syndrome).
• Iliac or common femoral stenosis: thigh and calf claudication, absent/weak femoral pulses in affected limb.
• Femoro-popliteal stenosis: calf claudication only, absent popliteal and distal pulses.
Neurological
Cauda equina
Elderly patients, history of chronic back pain, pain is bilateral and in the distribution of the S1–S3 dermatomes, may be
accompanied by paraesthesia in the feet and loss of ankle jerks, all peripheral pulses palpable and legs well perfused.
Stage of intermittent cluadication:

Stage I: Leg pain occurs during hard exercise
Stage II a: Maximum walking distance before precipitation of pain is 200 meters.
II b: Pain occurs on walking less than 200 meters.
Stage III: Pain occurs on walking a short distance and at rest.
Stage IV: Pain at Rest with clear skin ulcers and gangrene.
Risk Factors for (I.C.):

1) Smoking 2) Hypercholesterolemia
3) Hypertension 4) Diabetes mellitus
5) Angina 6) Old Age

Managements:
Define the cause of claudication by investigations:
-FBC: exclude polycythaemia.

- Glucose: diabetes.
- Lipids: hyperlipidaemia.
- ABI: estimate of disease severity.
- ECG: coronary disease.
- Angiography: precise location and extent of disease, pre-procedure planning. Intravenous -easier, safer, larger
volume of dye. Intraarterial-lower dye volume, better images, higher risk of complications.
-Digital subtraction-best images of all.
- Duplex scanning beginning to be used instead of angiography.
Treat the cause by:
-Exercise & diatery modification lipid restriction, adding vitamin E and vitamin B3 supplementation.
-Thrombolysis, antithrombotic medication & arteriodilators as :
Angiotensin converting enzyme (ACE) inhibitors, beta-blockers, antiplatelet agents (aspirin and clopidogrel),
pentoxifylline and cilostazol (selective PDE3 inhibitor).
-Disc prolapse surgery.
-Surgeryindicated in severe cases with limb-threatening.
Manifestation of claudication:
Investigation:
Laboratory:
CBC
Polycythemia
Blood & Urine glucose level.
Lipid & cholesterol profile.
Urinalysis for renal impairment.
Clotting factors.
ECG for cardiac causes.
Imaging:
-CT Diagnostic Angiography showing the anatomic arterial circulation.

- Doppler Ultrasound of arteries study.
- Magnetic Resonance Angiography.
Diagnostic angiogram demonstrating total occlusion of the left limb of an aorto-bifemoral graft
Treatment & Intervention:
The management of acute limb ischemia include prehospital care , emergency care , consultation and
medication .
Prehospital Care :
Its Include :
 Control ABCs .
 Obtaining intra-venous access .
 Oxygen administration .
 Recording and examination of distal pulses , skin condition and neurological examination of the
affected extremities .
Emergency Care :
In Both embolic or thrombotic acute limb ischemia :
First , initiate a heparin infusion with the goal of increasing activated partial thromboplastin time to 1.5
times normal levels. Acute leg pain correlated with a cool distal extremity, diminished or absent distal
pulses, and an ankle blood pressure less than 50 mm Hg should prompt consideration of emergent surgical
referral. In some cases of emboli, intra-arterial thrombolytic agents may be useful.
Heparin :
 Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not
actively lyse but is able to inhibit further thrombogenesis. Prevents reaccumulation of clot after
spontaneous fibrinolysis.
 Dosing : 80U/kg IV bolus followed by infusion of 18U/kg/h .
 Interactions include Digoxin, nicotine, tetracycline, and antihistamines may decrease effects;
NSAIDs, aspirin, dextran, dipyridamole, and hydroxychloroquine may increase toxicity.
 Contraindication : sub acute bacterial endocarditis; active bleeding; history of heparin-induced
thrombocytopenia and hypersensitivity .
 Precautions in neonates , preservative-free heparin is recommended to avoid possible toxicity
(gasping syndrome) by benzyl alcohol, which is used as preservative; caution in severe hypotension
and shock; recent neurosurgery (within 6 wk), major surgery within 48 h, known bleeding diathesis,
childbirth within 24 h, thrombocytopenia .
Consultation :
Early surgical consultation in patients with acute limb ischemia is prudent. Treatment options include :
 Embolic Disease : emolectomy , or inta-arterial thrmbolysis .

 Thrombotic Disease : Intra-arterial thrmbolysis /angioplasty or bypass surgery .
Embolectomy :
 Can be performed under either general or local anaesthesia

 Display and control arteries with slings
 Transverse artereotomy performed over common femoral artery
 Fogarty balloon embolectomy catheters used to retrieve thrombus (used for iliac, femoral, or
popliteal emboli )
 If embolectomy fails - on-table angiogram and consider
 Bypass graft or intraoperative thrombolysis

Intra-arterial Thrombolysis :
 Arteriogram and catheter advanced into thrombus

 Streptokinase 5000u/hr + heparin 250u/hr
 Alternative thrombolytic agents include urokinase or tissue plasminogen activator (tPA)
 Repeat arteriogram at 6 -12 hours
 Advance catheter and continue thrombolysis for 48 hours or until clot lysis
 Angioplasty of chronic arterial stenosis may be necessary
 Success 60-70% but needs careful case selection
 Not suitable if severe neuro-sensory deficit
 Thrombolysis can be accelerated by:
 Pulse spray through multiple side hole catheter

 Aspiration thrombectomy - debulking thrombus aspiration
 High dose over shorter time
 Complications :Mortality of 1-2% ,Bleeding - CVA, retroperitoneal
In Patient With significant aortoiliac disease , usually treated by aortobifemoral bypass. Its 5-year patency
rate is approximately 90%. Those patients in whom PVD becomes significant, however, often have a
plethora of comorbid medical conditions, such as cardiovascular disease, diabetes, and chronic obstructive
pulmonary disease, which increase procedural morbidity and mortality. Axillobifemoral bypass and femoral-
femoral bypass are alternatives, both of which have lower 5-year patencies but have lower procedural
mortality.
Some areas of arteriostenosis can be revascularized with percutaneous transluminal coronary angioplasty
(PTCA). If the occlusion is complete, a laser may be useful in making a small hole through which to pass the
balloon.
Medications :
Anticoagulants reduce thrombin generation and fibrin formation and minimize clot propagation.
Follow Up , advice the patient to stop smoking , avoid cold exposure and medication that lead to
vasoconstriction , including the medication used for migraines and over-the-counter medication . And
Patient education .
Compartment Syndrome :
increased pressure within a limited space compromises the circulation and function of the tissues
within that space . It may occur in extremities subjected to prolonged periods of ischemia followed by
reperfusion suffer reperfusion injury manifesting as both intracellular and interstitial edema. Typical clinical
findings of early compartment syndrome are severe pain that is disproportionate to the relative paucity of
physical findings. Patients usually have marked tenderness on compression of the edematous calf and severe
discomfort on passive extension of the calf with dorsiflexion or plantarflexion of the foot. As compartmental
pressure reaches 30 mm Hg, capillary perfusion is impaired and neurologic and muscular injury occurs.
21% incidence are due to vascular causes rises to 50% in patients with both popliteal and venous injuries .
Two incision, four-compartment fasciotomy is preferred by most of surgeons . Severe compartment
syndrome is manifest by an immediate pouting of the muscles as they swell beyond the fascial incision. The
skin incision should be long enough to prevent any restriction on the underlying muscle. When patients
undergo revascularization after a prolonged interval (6 hours or more) of severe ischemia, consideration for
a prophylactic fasciotomy in anticipation of impending compartment syndrome should be entertained.
Indications for surgery in ALI:
Immediately limb-threatening ischemia (class IIb and early class III) is preferentially treated surgically.
Interventions:
-Embolectomy:
A groin incision is made & the common femoral artery is opened. The clot is found in the artery a balloon catheter is
passed in turn into the proximal & distal arteries the balloon is inflated & the catheter withdrawn removing the clot.
- Angioplasty Balloons.
Balloon catheter used to withdrawn an acute thrombotic occlusion
-Endarterectomy.
- Stents & Arterial bypass graft
Vein graft used to bypass the site of arterial occlusion
-Percutaneous aspiration thrombectomy (PAT)
-Percutaneous mechanical thrombectomy (PMT)

Angiojet thrombectomy system
Direct surgical thrombectomy and closure of arteriotomy with patch angioplasty
-Surgical revascularization.
-Fasciotomy.
-Amputation.
See figure 24: Ideal Management of ALI

Complications:
-Relapse of the embolus, or, atheroma & thrombosis.
-Infections mainly staphillococci.
-Hemorrhage.
These complications however can be controlled by reducing the lipid intake through dietary restriction &
adding heparin to the arterial lines for decreasing the incidence of thrombosis. Changing frequently the
tubing line increases the chances of infection.
Death.
Amputation of the limb
Conclusion:
Atherosclerosis, the major cause of limb ischemia, is a global phenomenon. As such, attention should be directed not only to
the limb at risk but to the patient as whole. Hence, modification of systemic risk factors must play an important role in the
long-term care of these patients.
References:
1-Medscape article of Acute limb ischemia .
2-Baily & Love short practice of surgery 25th ED CH: 53 Arterial disorders.
3-Schwartz’s principles & practice of surgery 9th ED CH: 23 Arterial Diseases.
4-Richard Snell Clinical Anatomy 7th ED CH:10 The Lower Limb.
5-Pierce A. Grace, & Neil R. Borley et al, Surgery at a Glance 2nd ED, by Blackwell Publishing company, Part 1 Clinical
presentation at glance ,20 Claudication.
INTRAPERITONEAL HEMORRHAGE
Differential Diagnosis, & Management
AC:207002113
Group : B3
SUPERVISIED BY DR.GR VERMA
INTRAPERITONEAL HEMORRHAGE DIFFERENTIAL DIAGNOSIS & MANAGEMENT
Introduction:
In order to know the different causes of intraperitoneal hemorrhage you should have a good knowledge about the
peritoneal cavity & its function.
Anatomy of the peritoneum:
It is a thin serous membrane lining the walls of abdominal & pelvic cavities and covering the abdominal and Pelvic
viscera. The parietal peritoneum lines walls of abdominal & pelvic cavites & visceral peritoneum covers the organs.
The potential space between parietal &visceral Layers is called the Peritoneal cavity.
The peritoneal cavity is divided into two main spaces:
I- The greater sac:
It is the cavity opened when the anterior abdominal wall is opened.
II- The lesser sac:
It is a separate cavity present mainly behind the stomach.
It communicates with the greater sac through an opening lying behind

the right free border of the lesser omentum. This opening is called
epiploic foramen (Foramen into lesser sac).
Intraperitoneal Organs:
-Liver.
-Spleen.
-Stomach.
-Small intestine.
-Large intestine except descending colon,rectum & the anal canal.
-Uterus.
Retroperitoneal organs:
-Pancreas.
-Abdominal Aorta.
-Third part of the duodenum.
-Descending colon, rectum & the anal canal.
-Kidneys.
-Ureters.
Function:
-Mobility of the visceral organs.
-Defense specially during inflammation.

-Localisation of the infection tipically seen in appendicitis(Policeman of the abdomen).
-Protection of the visceral organs.
-The peritoneal folds suspend the various organs within the peritoneal cavity and convey the blood vessels, lymphatic
vessels and nerves to these organs.
-Storage of fats.
Definition:
Intraperitoneal Hemorrhage (Hemoperitonum, Hematoperitonum, or IPH):
Presence of blood in the peritoneal cavity. The blood accumulates in the space between the inner lining of the abdominal wall and
the internal abdominal organs. In general Intrapertoneal hemorrhage is classified as a surgical emergency which needs laparotomy
to identify & control the source of bleeding.Due to this bleeding distention of the abdominal wall take place. But this occurs later
while the initial complication is hemorrhagic shock .
Epidemiology:
-Abdominal injuries are present in 7-10% of traumatic patients.
Blunt trauma:
1. Spleen (45%)
2. Liver (40%),
3. Retroperitoneal haematoma (15%).
-Blunt abdominal trauma is very common in road traffic accidents.
-Penetrating trauma: these may be:
-Stab wounds and low velocity gunshot wounds: cause damage by laceration or cutting. Commonly involve:
1. liver (40%)
2. small bowel (30%)
3. diaphragm (20%)
4. colon (15%);
- High velocity gunshot wounds transfer more kinetic energy and also cause further injury by cavitation
effect, tumble, and fragmentation. Commonly involve
1. Small bowel (50%)

2. Colon (40%)
3. Liver (30%)
4. Vessels (25%).
-Trauma is the leading cause of death to age less than 45 years, the fourth leading cause overall, and leading
contributor to years of potential life lost (YPLL) before age 65.
-Modern trauma care is derived from care of wounds and casualty management during major wars.
-Trauma deaths occur at three time periods following injury, each having a unique pattern and etiology: 50%
at the scene, 30% within the golden hours or acute resuscitation phase, and 20% delayed from several days
to several weeks after injury.
Prevention of Trauma caused by Traffic accidant:
-Seat belt use is very important as it reduce the injuries.
Causes:
-Penetrating abdominal & pelvic trauma.
-Blunt trauma, causing injuries to solid organs such as the liver and spleen.
-Vascular accidents, such as rupture of an Abdominal aortic aneurysm, Iliac Aneurysm, or Splenic Aneurysm.
-Big course of Anticoagulant(Warfarin, Heparin)
- Ruptured ectopic pregnancy
- Uterine rupture.
-Rupture of uterine cyst.
-Post operative bleeding.
-Intraoperative bleeding.
-Rupture of tuberculous pelvic abscess.
-Rupture of intraperitoneal abscess.
- Bleeding due to a perforated Peptic ulcer.
-Gastric erosions.
-Zollinger Elleson syndrome.
-Gastric cancer.
-Rupture of hepatic hemangioma.
-Rupture of Hematoma of the liver
-Rupture of malarial spleen.
-Angiodysplasia.
-Perforated Meckel’s diverticulum
-Crohn’s & ulcerative colitis.
-Peutz-Jeghers syndrome.
-Intestinal obstruction.
-Ovarian cyst rupture
-Adnexal torsion
- Rupture of Hepatoblastoma.
-Rupture of corpus luteum hematoma
-Disseminated intravascular coagulation.
-Acute Hemorrhagic pacreatitis.
Classification of IPH: It depends on the percentage of volume hemorrhage of Blood:

-Class I: mild usually compensated hemorrhage up to 15 % of blood volume. There is typically no change
in the vital signs and fluid resuscitation is not usually necessary.
-Class II : moderate involves 15-30% of total blood volume. A patient is often tachycardic with a
narrowing of the difference between the pulse pressure. The body attempts to compensate with peripheral
vasoconstriction. Skin may start to look pale and be cool to the touch. The patient may exhibit slight
changes in behavior.
-Class III: moderate involves loss of 30-40% of circulating blood volume. The patient's blood pressure
drops, the heart rate increases, shock develops, such as capillary refill worsens, and the mental status
worsens. Fluid resuscitation with crystalloid and blood transfusion are usually necessary.
-Class IV: severe hemorrhage that involves loss of >40% of circulating blood volume. The limit of the body's
compensation is reached and aggressive resuscitation is required to prevent death.
Pathophysiology:
-Traumatic Injuries (stab wound, penetrating ,& blunt)
-Inflammation & infection(eg.Hb pylori and gastric ulcer, Idiopathic inflammatory bowel diseases)
-Perforation (Peptic ulcer, perforated viscus)
-Tumor process:
1-Bengin(Hemangioma, leimyoma)
2-Malignancy(Hepatoblastoma, peritoneal carcinomatosis)
-Vascular(Aneurysm, hematoma,Dissection, Intestinal ischemia)

-Gynecological(Ectopic pregnancy, uterine rupture ovarian cyst, ruptured abscesses)
-Obstruction(Intestinal obstruction)
-Strangulation.
-Drugs(NSAIDs, Anticoagulant)
Clinical Presentation:
Haemoperitoneum is best considered as falling into two categories: progressive and stable.
Progressive IPH:
-Progressive haemoperitoneum implies active continued intra-abdominal bleeding and is most commonly encountered with
injuries to the solid organs (liver and spleen).
- Signs of hypovolaemic shock.
- Progressive distension of the abdomen( which in severe injuries involving major vessels (e.g. hepatic veins) may become so
tense as to obstruct venous return from the lower limbs).
- Postoperative bleeding .
-Reactionary bleeding occurs from cut small blood vessels that are missed at operation .
-Bleeding from an arterial anastomosis may also be the result of infection.
. Thesepatients only survive with prompt resuscitation and immediate surgical intervention.
Stable IPH:
- A stable haemoperitoneum implies that the lesion which caused the haemoperitoneum in the first instance is no longer actively
bleeding.
- The manifestations of patients with stable haemoperitoneum are not always clear.
-Shifting dullness can sometimes be elecited.
-Raising the lower limb with the body in supine position leads to accumulation of fluids in subphrenic recess that leads to peritoneal
irritation & shoulder pain.
History:
Most of the time the patient come with a history of an abdominal pain so obtain as detailed a history as possible regarding the
time of onset, duration, intensity, and character of the pain and any associated symptoms. Also in pregnant female ask about the
menstrual history for assessment of pregnancy associated diseases. History of urinary symptoms as hematuria, frequency
micturation, pain in the groin region. History of vascular symptoms as throbbing pain or pulsatile swelling, stabbing pain. History
of trauma to the abdomen, or pelvis. History of malignancy as hepatoblastoma.
History of liver biopsy as some times liver biopsy is associated with bleeding. History of peptic ulcer.
Surgical History in the abdomen in the latest years.
Drug history as anticoagulant, NSAIDs. History of travel to malaria endemic areas.
Family history of a similar condition, & there diagnosis.
Physical Examination:
General examination is important for obtaining the vital signs , posture of the patient as those with colicy pain.
Observation
• Bending Forward: Chronic Pancreatitis
• Jaundiced: CBD obstruction
• Dehydrated: Peritonitis, Small Bowel obstruction

• -INSPECTION for distention, shape of the abdomen, scars of previous surgery, masses, rash, pigmentation.
• -AUSCULATION for hyperactive, obstructive, absent, or normal bowel sounds.
• -PALPATION to look for guarding, rigidity, rebound tenderness, organomegally, or hernias.
• AUSCULTATION. For bruit
• Do not forget to do Rectal examination specially when associated with intraluminal gastrointestinal hemorrhage
• Women should have pelvic exam or Per-vaginal exam
Differential diagnosis:
 Gastrointestinal
o Acute hemorrhagic pancreatitis
o Peptic ulcer perforation
o Perforation of crohn’s disease
o Splenic rupture.
o Bowel obstruction, & perforation
o Herniation, & strangulation
o Acute rupture of cholecystitis.
o Meckel diverticulitis rupture
o Pancreatic pseudocyst rupture
o Hepatoblastoma
o Hepatic hemangioma,& adenoma
o Abdominal Trauma
o Zollinger Elleson syndrome.
o Gastroesphageal stromal tumor.
 Genitourinary
o Ovarian cyst rupture
o Uterine rupture
o Adnexal torsion
o Rupture of renal pelvis
o Ureteral obstruction
o Rupture of corpus luteum, or hematoma
 Vascular
o Superior mesenteric artery syndrome
o Rupture of gastroepiploic artery.
o Thrombosis/infarction - Specifically mesenteric venous thrombosis
o Ruptured visceral artery aneurysm
o Splenic artery aneurysm
o Ruptured aortic aneurysm.
o Ruptured hematoma
o Iliac artery aneurysm
o Polyarteritis nodosa
Conditions associated with pregnancy
 Rupture of rectus abdominis muscle

 Torsion of the pregnant uterus
 Pelvic Inflammatory disease (PID).
Due to pregnancy
 Early pregnancy
o Ruptured ectopic pregnancy
 Later pregnancy
o Torsion of pedunculated myoma
o HELLP (hemolysis, elevated liver function, and low platelets) syndrome – Spontaneous rupture of the liver.
o Uterine rupture
Complication of IPH:
Acute:
-Shock : usually in the form of hypovolaemic shock.
-Renal failure.
-Peritonitis.
-Peritoneal rupture.
-Death.
Chronic:
-Anemia.
-Jaundice.
-Infirtility in females of gynecologic diseases.
Investigations:
Lab:
-CBC, Hb,DLC for infection.

-Electrolytes : (Na, & K).
-Amylase , lipase for pancreatitis.
-Liver function test:
1-PT(Prothrombin time), PTT(Partial thromboplastin time).
2-Alkaline phosphatase.
3-ALT, AST.
-Urinalysis Urea,,Nitrogen.
-Tumor markers as (AFP), Gene analysis for specific tumors.
Imaging:
-Plane abdominal x-ray (showing obstruction, calcification, uretric calculi, air, fluids).
-Ultrasound shows almost all the abdominal pathology.
-Arterial Angiography.
-MRI for soft tissue change.
-CT Scan for lymphnodes state, & associated metastasis.
Special tests:
-Gastrointestinal Tract Endoscopy for ulcers detection.
-Biopsy confirming the disease.
-Focused assessment with sonography for trauma (FAST).
-Paracentesis or Diagnostic peritoneal lavage (DPL).
-Computed tomography(CT Scan).
-Diagnostic laparoscopy or exploratory laparotomy
Treatment:
In case of trauma:
Initial OR Primary Assessment: ABCDE
Assessment of the airway, breathing, circulation, disability, exposure and level of consciousness of the patient by
(GCS).
1-Assessment of Airways:
Airway obstruction often responds to simple maneuvers such as suctioning, chin lift, jaw thrust, or placement of an
oropharyngeal airway. Persistence of respiratory insufficiency requires endotracheal intubation. Unsuccessful
intubation necessitates cricothyroidotomy. Occasionally, the anatomy does not allow cricothyroidotomy, as can occur
with laryngeal fracture. In these cases, a formal tracheotomy must be performed. After an airway is established, a
physician auscultates the chest to confirm air exchange, confirms return of carbon dioxide via the endotracheal
tube and obtains a chest radiograph to ensure proper tube position with the tip proximal to the carina. Appropriate
placement of endotracheal tubes inserted in the prehospital setting should also be confirmed at this time.
2-Assessment of Breathing:
Ensure adequate ventilatory exchange by rapid auscultation of both lung fields and assessment for mechanical
factors that may interfere with breathing(Foreign body) . These factors include compression of the lung from
hemothorax, pneumothorax, or visceral herniation; loss of chest wall stability from flail chest; lung damage from
pulmonary contusion; and airway obstruction from aspiration. A dramatic presentation with cyanosis, intense
respiratory effort without air movement, distended neck veins, and lack of breath sounds on chest auscultation
indicates that a tension pneumothorax is present. Clinical diagnosis of tension pneumothorax requires immediate
needle thoracostomy followed by chest tube thoracostomy. Sucking chest wounds should be sealed with an occlusive
dressing secured on three sides to function as a flap valve. Most other problems become evident on the initial chest
radiograph and are relieved by chest tube insertion, suctioning, or repositioning of the endotracheal tube. The optimal
position for chest tube insertion is the midaxillary line at the fifth or sixth interspace, avoiding the axilla, the large
muscles of the back and chest, and the breast. Insertion of a finger into the chest before chest tube placement ensures
entry into the pleural space and provides the opportunity to search digitally for defects in the diaphragm.
3-Assessment of Circulation:
Circulatory status can be measured by: Blood pressure, pulse, skin perfusion, temperature, capillary refill,
mental status, presence of breath sounds, and neck vein distention. The first issue is to establish whether
the patient is in hypovolemic shock and, if so, to determine the source of hemorrhage. Circulatory collapse
in the injured patient is almost always caused by hypovolemia secondary to hemorrhage. Occasionally,
concurrent heart disease, spinal cord injury, or cardiac tamponade may contribute. The mainstay of
treatment for hypotension in the injured patient, regardless of cause, is volume resuscitation with crystalloid
solution and, if hypotension is persistent, packed red blood cells (RBCs, or Transfusion). A lack of
response to IV infusion of 2 L of lactated Ringer's solution indicates significant, ongoing hemorrhage
and necessitates immediate blood transfusion.
The less responsive a patient is to initial volume resuscitation, the more urgent is the need for
hemorrhage control. One need not wait for a response to resuscitation before taking the patient to the
operating room. Another situation that requires vigilance is the cool, pale patient with relatively normal vital
signs. These patients are compensating maximally and have a normal blood pressure because of intensive
peripheral vasoconstriction. However, this compensatory mechanism is of only limited duration, and such
patients require immediate rapid volume transfusion, blood transfusion, and operative control of bleeding. A
similar trap exists for patients with the mangled extremity syndrome or multiple open fractures. Patients may
have lost significant blood volume at the injury scene. Before resuscitation, there may be relatively little
hemorrhage from the open wounds; however, initiation of IV fluids may increase blood pressure and cause
vasodilation, resulting in increased hemorrhage. These patients require immediate volume resuscitation and
operative control of their wounds.
4-Assessment of the degree of disability.
5-Assessment of the exposure.
6-Assessment of Level of consciousness:
A brief neurologic evaluation to assess the components of the GCS .The GCS is scored by assessing eye opening,
verbal responses, and motor responses with a maximal (normal) score of 15.
Glasgow Coma Scale

DIAGNOSTIC GLASGOW COMA SCALE (GCS)
EYE OPENING
Spontaneous 4
To voice 3
To pain 2
None 1
VERBAL RESPONSE
Oriented 5
Confused 4
Inappropriate words 3
Incomprehensible sounds 2
None 1
MOTOR RESPONSE
Obeys commands 6
Purposeful movement (pain) 5
Withdraw (pain) 4
Flexion (pain) 3
Extension (pain) 2
None 1
GCS SUBTOTAL 3 - 15
GCS of 8 or less has been used as an alternative definition of coma. This definition is valid, however, only when
associated with the absence of eye opening to verbal command.
Secondary Assessment:
The secondary survey is directed at specific identification of suspected and unsuspected injuries. It consists of a
thorough physical examination that includes observation and palpation of:
-Head & Neck.
-Chest.
-Abdomen.
-Pelvis.
-Extremities.
Medical Treatment: Resusitative or conservative treatment
-Blood transfusion.
-Rehydration.
-Antibiotics.
Surgical Treatment:
The purpose of surgery to control the source of bleeding examples of surgery:
-Splenectomy.
-Ligation & clamping of arteries.
- Bleeding liver might be controlled by application of hemostatic sponges, thrombin, or, argon beam cauterization.
-Endovascular surgery in case of Rupture aortic aneurysm.
-Laparotomy is the most common surgery.
-Open abdominal surgery.
-Sometimes observation is indicated.
Note:
-Progressive haemoperitoneum requires immediate surgical intervention with volume replacement (blood, colloids and crystalloids)
during the surgery. The primary aim of the operation is to control the bleeding.
- Patients with stable haemoperitoneum should be investigated without delay and some will require urgent surgical treatment when the
diagnosis is confirmed.
Indications for surgery for a bleeding duodenal ulcer

Timing Age Basis of decision
(years)
Immediate Any Uncontrollable spurting vessel at endoscopy
Clinical exsanguination
Delayed Over 60 More than 4 units of blood required for haemodynamic stabilisation or more than 8 units over 48
hours
Under 60 More than 8 units necessary for stabilisation or more than 12 units needed over 48 hours
On Over 60 One rebleed after initial successful control but while still in hospital
rebleeding
Under 60 Two rebleeds after initial successful control but while still in hospital
BLUNT ABDOMINAL TRAUMA: INDICATIONS FOR LAPAROTOMY
-Unstable and abdominal injury is highly suspected (positive FAST ultrasound)
-Pneumoperitoneum
-Diaphragm rupture seen on CXR
-Blood per nasogastric tube, rectum, or in vomitus
-Peritoneal signs
ANTERIOR ABDOMINAL STAB WOUND: INDICATIONS FOR LAPAROTOMY
-Instability
-Peritoneal signs
-Upper abdomen or epigastrium (consider intrathoracic injury or pericardial tamponade)
-Blood from nasogastric tube
-Evisceration
-Suspected diaphragm injury
Indications for urgent laparotomy
 Blunt trauma with positive DPL or free blood on ultrasound and an unstable circulatory status.
 Blunt trauma with CT features of solid organ injury not suitable for conservative management.
 Clinical features of peritonitis.
 Any knife injury associated with visible viscera, clinical features of peritonitis, haemodynamic
instability, or developing fever/signs of sepsis.
 Any gunshot wound.
Prognosis:
It depends on three things:
-Early diagnosis. Amount of blood loss, stability of the case.
-Cause of hemorrhage. Tumor, vascular malformation.
-Personal dependency: specially age certain ages are at high risk of developing complications.
So if the patient detected early the prognosis usually is good.
If the patient was detected lately with severe hemorrhage usually the patient recover with a sort of disability.
In patient detected with ruptured tumors if localized good prognosis if metastasize poor prognosis.
REFERENCES:
1-Greenfield's Surgery: SCIENTIFIC PRINCIPLES AND PRACTICE, 4th Edition, CH: 16,17,18,25. By LWW.
2-Last Minute Emergency Medicine a concise review for speciality board by Mary Jo Wagner,& Susan B. Promes
,MC graw hill MEDICAL.
3-Clinical Surgery 2nd ED by Kumar & Clark by Elesiver Philadelphia.
4- ACS .SURGERY PRINCIPLES & PRACTICE 2007 6th ED BY The Amarican College of Surgeon.
5-Clinical Surgery 2nd ED by Blackwell science publishing company.

Potentially Life-Threatening Causes which leads to hemoperitonium of Abdominal Pain
Cause Epidemiology Etiology Presentation Physical Useful Tests
Examination
Ruptured Occurs only in females Risk factors include Severe, sharp Shock or evidence of bHCG testing
ectopic of childbearing age nonwhite race, older constant pain peritonitis may be necessary for all
pregnancy without bilateral age, history of STD or localized to the present. Lateralized women of childbearing
(critical) oophorectomy. No PID, infertility affected side. More abdominal ages (10–55). This
method of treatment, intrauterine diffuse abdominal tenderness. Localized combined with
contraception prevents contraceptive device pain with adnexal tenderness or ultrasonography,
ectopic pregnancy. within the last year, intraperitoneal cervical motion preferably
Approximately 1 in tubal sterilization, and hemorrhage. Signs tenderness increase transvaginal, is usually
every 100 pregnancies. previous ectopic of shock may be the likelihood of diagnostic.
pregnancy. present. Midline ectopic pregnancy. Culdocentesis reserved
pain tends not to be Vaginal bleeding for circumstances
ectopic pregnancy. does not have to be where other more
present. sophisticated testing is
not available.
Ruptured or Incidence increases Atherosclerosis in Patient often Vital signs may be Abdominal plain films
leaking with advancing age. over 95%. Intimal asymptomatic until normal (in 70% of abnormal in 80% of
abdominal More frequent in men. dissection causes rupture. Acute patients) to severely cases. Lateral
aneurysm Risk factors include aortic dilatation and epigastric and back hypotensive. abdominal film may
(critical) HTN, DM, smoking, creation of a false pain often associated Palpation of a be helpful. Ultrasound
COPD, and CAD. lumen. Leakage or with or followed by pulsatile mass is can define diameter
rupture causes shock. syncope or signs of usually possible in and length but limited
shock. Pain may aneurysms 5 cm or by obesity and gas.
radiate to back, greater. If suspected, Spiral CT test of
groin, or testes. the physical choice if patient is
examination should stable.
not be relied on only.
CT or US usually
indicated. Bruits or
inequality of femoral
pulses may be
evident.
Mesenteric Occurs most 20%–30% of lesions Severe pain, colicky, Early examination Often a pronounced
ischemia commonly in elderly are nonocclusive. The that starts in results can be leukocytosis is
(emergent) people with CV causes of ischemia are periumbilical region remarkably benign in present. Elevations of
disease, CHF, cardiac multifactorial, and then becomes the presence of amylase and creatine
dysrhythmias, DM, including transient diffuse. Often severe ischemia. phosphokinase levels
sepsis, and hypotension tension in associated with Bowel sounds often are seen. Metabolic
dehydration. the presence of vomiting and still present. Rectal acidosis due to lactic
Responsible for 1 of preexisting diarrhea. examination acidemia is often seen
1000 hospital atherosclerotic lesion. important because with infarction. Plain
admissions. Mortality The arterial occlusive mild bleeding with films of limited
70%. Mesenteric causes (65%) are positive guaiac stools benefit. CT, MRI, and
venous thrombosis secondary to emboli can be present. angiography are
associated with (75%) or acute arterial accurate to varying
hypercoagulable states, thrombosis (25%). degrees.
hematologic
inflammation, and
trauma.
Intestinal Peaks in infancy and Adhesions, carcinoma, Crampy diffuse Vital signs usually WBC count may
obstruction elderly. More common hernias, abscesses, abdominal pain normal unless indicate strangulation
(urgent) with history of volvulus, and associated with dehydration or bowel if elevated.
previous abdominal infarction. Obstruction vomiting. strangulation has Electrolytes may be
surgery. leads to vomiting, occurred. Abdominal abnormal if associated
third spacing of fluid, distention, with vomiting or
strangulation, and hyperactive bowel prolonged symptoms.
necrosis of bowel. sounds, and diffuse Abdominal films are
tenderness. Local useful for identifying
peritoneal signs level of obstruction.
indicate US or CT rarely
strangulation. needed to make
diagnosis.
Cause Epidemiology Etiology Presentation Physical Useful Tests
Examination
Perforated Incidence increases More often a duodenal Acute onset of Fever, usually low WBC count usually
viscus with advancing age. ulcer that erodes epigastric pain is grade, is common, elevated due to
(urgent) History of peptic ulcer through the serosa. common. Vomiting higher fever occurs peritonitis. Amylase
disease or diverticular Colonic diverticula, in 50%. Fever may with time. may be elevated as
disease common. large bowel, small be present later. Pain Tachycardia is well. LFT results are
bowel, and gallbladder may localize with common. Abdominal variable. Upright view
perforations are rare. omental walling off examination reveals of radiographs reveals
Spillage of bowel of peritonitis. Shock diffuse guarding and free air in 70%–80%
contents causes may be present with rebound. A of cases with
peritonitis. bleeding or sepsis. ―boardlike‖ abdomen perforated ulcers.
in later stages. Bowel
sounds are decreased.
Acute Peak age in adulthood. Alcohol, gallstones, Acute onset of Low-grade fever Lipase is test of
pancreatitis Rare in childhood and hyperlipidemia, epigastric pain common. Patient may choice. Amylase 3×
(urgent) elderly. Male hypercalcemia, or radiating to the be hypotensive or normal more specific
preponderance. endoscopic retrograde back. Nausea and tachypneic. Some for diagnosis.
Alcohol abuse and pancreatography vomiting common. epigastric tenderness Ultrasound may show
biliary tract disease are causes pancreatic Pain usually present. Since edema or pseudocyst.
risk factors. damage, disproportionate to retroperitoneal organ, CT scan may show
saponification, and physical findings. guarding or rebound abscesses, necrosis,
necrosis. ARDS, Adequate volume not present unless hemorrhage, or
sepsis, hemorrhage, repletion is severe. Flank pseudocysts. CT is
and renal failure are important in the ecchymoses may be ordered if severe acute
secondary. initial therapy. seen if hemorrhagic. pancreatitis is
suspected.
CAD, coronary artery disease; CHF, congestive heart failure; COPD, chronic obstructive pulmonary disease; CV, cardiovascular; DM, diabetes
mellitus; HTN, hypertension; PID, pelvic inflammatory disease; STD, sexually transmitted disease.
ACUTE ABDOMEN
DIFFERENTIAL DIAGNOSIS, & MANAGEMENT
AC: 207002113
GROUP: B3
GENERAL SURGERY ASSIGNMENT

ACUTE ABDOMEN
Definition:
"any serious acute intra-abdominal condition attended by pain, tenderness, and muscular rigidity, abdominal guarding,
i
and for which emergency surgery must be considered."
Note:
The approach to pregnant patients with severe abdominal pain is very similar to that for nonpregnant patients with
acute abdomen. However, the physiologic changes associated with pregnancy must be considered when interpreting
findings from the history and physical examination.
Pathophysiology:
Principal causes of abdominal pain are:
-Inflammation including infection (Ambiasis, gastroenteritis,

Idiopathic inflammatory bowel diseases).
-Perforation of the thickness of the GIT. (As in perforated

peptic ulcer, or perforated viscus).
-Obstruction of the viscus causing distention --- causing

visceral pain---- overdistention causes involvement of the
parietal peritoneum.
-Infarction or strangulation (mesenteric infarct).
-Intra & retro peritoneal hemorrhage (Acute hemorrhagic

pancreatitis).
-Injury what ever the cause as trauma(Stabbing specially in

pregnant females).
-Extra-abdominal causes as a referred pain in:
1- MI
2-DKA (Diabetic Ketoacidosis).
3-Bilateral Pleurisy.
Types of pain:
1-Visceral pain
-Distention, inflammation or ischaemia in hollow viscous & solid organs
-Localisation depends on the embryologic origin of the organ:
• Forgut to epigastrium
• Midgut to umbilicus
• Hindgut to the hypogastric region
2-Parietal pain
It is localised to the dermatome above the site of the stimulus.
3-Referred pain
produces symptoms, no signs of tenderness.
Classification of pain in the abdomen:
1-According to systems.
1. Intra-abdominal (arising from within the abd cavity / retroperitoneum) involves:
-Gastrointestinal (Appendicitis, Diverticulitis)
-Genitourinary (Renal Colic)
-Gynaecology (Acute PID, Pregnancy)
-Vascular systems (AAA, Mesenteric Ischemia)
2. Extra-abdominal (less common) involves:
-Cardiopulmonary (AMI)
-Abdominal wall (Hernia, Zoster)
-Toxic-metabolic (DKA, lead)
-Neurogenic pain (Zoster)
Psychic or psychosomatic (Anxiety, Depression)
3. Nonspecific Abdminal pain – not well explained or described.
2-According to abdominal quadrants.
-Anatomicaly 9 quadrants.
-Surgicaly 4 quadrants.
3-Upper & Lower abdomen.
4-Generalized & Localized or central.
History:
Obtain as detailed a history as possible regarding the time of onset, duration, intensity, and character of the pain and
any associated symptoms. Also in married female asking about the menstrual history for assessment of pregnancy &
its associated diseases. Remember that nausea, vomiting, constipation, increased frequency of urination, and pelvic
or abdominal discomfort are frequently experienced in normal pregnancy.
Also consider the site of the pain in relation with anatomical quadrants of the abdomen & also radiation, shifting, or
referred pain.
Relieving & exacerbating factors.
History of urinary symptoms as hematuria, frequency micturation, pain in the groin region.
History of vascular symptoms as throbbing pain or pulsatile swelling stabbing pain.

Occupations as those exposed to lead.
Sites of pain in the abdomen:
Generalized abdominal pain:
• Perforation
• Abdominal aortic anyresm(AAA)
• Acute pancreatitis
• Diabetes mellitus
• Bilateral pleurisy
Central abdominal pain:
• Early appendicitis
• Acute gastritis
• Ruptured AAA
• Mesenteric thrombosis
Epigastric abdominal pain:
• Dudenal or Gastric ulcer
• Oesophagitis
• AAA
Right Upper Quadrant (RUQ) pain:
• Gallbladder disease
• Dudenal ulcer
• Pneumonia
• Subphrenic abscess
Left Upper Quadrant (LUQ) pain:
• GU
• Pneumonia
• Spontaneous splenic rupture
• Acute perinephritis
• Subphrenic abscess
Suprapubic abdominal pain:
• Acute urinary retention
• UTIs
• Cystitis
• PID
• Ectopic pregnancy
• Diverticulitis
Right iliac fossa pain:
• Acute appendicitis
• Mesenteric adenitis (young)
• Perf DU
• Diverticulitis
• PID
• Salpingitis
• Ureteric colic
• Meckel’s diverticulum
• Crohn’s disease
• Biliary colic (low-lying gall bladder)
Loin pain:
• Muscle strain
• UTIs
• Renal stones
• Pyelonephritis
Left iliac fossa pain:
• Diverticulitis
• Constipation
• Irittable bowel syndrome
• PID
• Rectal Carcinoma
• UC
Ask detailed history of the pain as these questions:
 Did the pain begin suddenly or did it grow in intensity?

 Is it steady or crampy, dull and aching, or sharp and stabbing?
 Did it occur before or after a meal?
 Did it awaken the patient from sleep?
 How well is it localized, and has the location changed?
 Is it associated with nausea and vomiting; and, if so, did these begin before or after the pain?
 Does anything make the pain worse, or make it better?
Ask about the past history of similar attack or diseases that are chronic.
Past surgical history.
Drug history specially steroids, & NSAIDs, drug allergy, food allergy.
Family history of a similar condition, & there diagnosis.
Associated symptoms & constitutional symptoms should be rolled out.
Systemic review :
Especially concerning the chief complaints, disease process & complications.
By the end of history initial diagnostic possibilities are rolled out.
General examination is important for obtaining the vital signs , posture of the patient as those with colicy pain.
Observation
• Bending Forward: Chronic Pancreatitis
• Jaundiced: CBD obstruction
• Dehydrated: Peritonitis, Small Bowel obstruction
Note: Abdominal examination is preverably done by surgeon to roll out the severe forms of diseases first then if
stabilized admitted to either surgical or medical unit.
Abdominal examination:
-INSPECTion for distention, shape of the abdomen, scars of previous surgery, masses, rash.
-AUSCULATion for hyperactive, obstructive, absent, or normal bowel sounds.
-PALPATION to look for guarding, rigidity, rebound tenderness, organomegally, or hernias.
-Women should have pelvic exam or Per-vaginal exam (check FHR if pregnant):
• Bleeding
• Discharge
• Cervical motion tenderness
• Adnexal masses or tenderness
• Uterine Size or Contour
-Men should have pelvic scrotal exam.
-Anyone with a rectum should have per-rectal exam:
• tenderness
• induration
• mass
• frank blood
Important Signs in Patients with Abdominal Pain
Sign Finding Association
Cullen's sign Bluish periumbilical Retroperitoneal haemorrhage

discoloration
Kehr's sign Severe left shoulder pain Splenic rupture

Ectopic pregnancy rupture
McBurney's sign Tenderness located 2/3 distance from Appendicitis

anterior iliac spine to umbilicus on right side
Murphy's sign Abrupt interruption of inspiration on Acute cholecystitis

palpation
of right upper quadrant
Psoas sign Hyperextension of right hip causing Appendicitis

abdominal pain
Obturator's sign Internal rotation of flexed right hip causing Appendicitis

abdominal pain
Grey-Turner's Discoloration of the flank Retroperitoneal haemorrhage

sign
Chandelier sign Manipulation of cervix causes patient to lift Pelvic inflammatory disease
buttocks off table
Rovsing's sign Right lower quadrant pain with palpation of Appendicitis

the left lower quadrant
Summary of Important causes of abdominal pain:
-Pain Originating in the Abdomen

Parietal peritoneal inflammation
Bacterial contamination
 Perforated appendix or other perforated viscus
 Pelvic inflammatory disease
Chemical irritation
 Perforated ulcer
 Pancreatitis
 Mittelschmerz
Mechanical obstruction of hollow viscera
 Obstruction of the small or large intestine
 Obstruction of the biliary tree
 Obstruction of the ureter
Vascular disturbances
 Embolism or thrombosis
 Vascular rupture
 Pressure or torsional occlusion
 Sickle cell anemia
Abdominal wall
 Distortion or traction of mesentery
 Trauma or infection of muscles
Distension of visceral surfaces, e.g. by
hemorrhage
 Hepatic or renal capsules
Inflammation of a viscus
 Appendicitis
 Typhoid fever
 Typhlitis
-Pain Referred from Extraabdominal Source
Cardiothoracic
 Acute myocardial infarction
 Myocarditis, endocarditis, pericarditis
 Congestive heart failure
 Pneumonia
 Pulmonary embolus
 Pleurodynia
 Pneumothorax
 Empyema
 Esophageal disease, spasm, rupture, inflammation
Genitalia
 Torsion of the testis
-Metabolic Causes
 Diabetes
 Uremia
 Hyperlipidemia
 Hyperparathyroidism
 Acute adrenal insufficiency
 Familial Mediterranean fever
 Porphyria
 C′1 esterase inhibitor deficiency (angioneurotic edema)
-Neurologic/Psychiatric Causes
 Herpes zoster
 Tabes dorsalis
 Causalgia
 Radiculitis from infection or arthritis
 Spinal cord or nerve root compression
 Functional disorders
 Psychiatric disorders
-Toxic Causes
Lead poisoning
Insect or animal envenomations
 Black widow spiders
 Snake bites
-Uncertain Mechanisms
Narcotic withdrawal
Heat stroke
Differential diagnosis:
 Gastrointestinal
o Acute appendicitis
o Acute pancreatitis
o Peptic ulcer
o Gastroenteritis
o Hepatitis
o Bowel obstruction
o Bowel perforation
o Herniation
o Meckel diverticulitis
o Toxic megacolon
o Pancreatic pseudocyst
 Genitourinary
o Ovarian cyst rupture
[20 ]
o Adnexal torsion
o Ureteral calculus
o Rupture of renal pelvis
o Ureteral obstruction
 Vascular
o Superior mesenteric artery syndrome
[21 ]
o Thrombosis/infarction - Specifically mesenteric venous thrombosis
o Ruptured visceral artery aneurysm
o Splenic artery aneurysm
 Respiratory
o Pneumonia
o Pulmonary embolism
 Other
o Intraperitoneal hemorrhage
o Splenic rupture
o Abdominal trauma
o Acute intermittent porphyria
o Diabetic ketoacidosis
o Sickle cell disease
Conditions associated with pregnancy
 Acute pyelonephritis
 Acute cystitis
 Acute cholecystitis
 Acute fatty liver of pregnancy
 Rupture of rectus abdominis muscle
 Torsion of the pregnant uterus
Due to pregnancy
 Early pregnancy
[17 ]
o Ruptured ectopic pregnancy
o Septic abortion with peritonitis
o Acute urinary retention due to retroverted gravid uterus
 Later pregnancy
o Red degeneration of myoma
o Torsion of pedunculated myoma
o Placental abruption
o Placenta percreta
o HELLP (hemolysis, elevated liver function, and low platelets) syndrome – Spontaneous rupture of the
liver
o Uterine rupture
o Chorioamnionitis
Differential diagnosis according to age:
Preschool-age
-Intussusception, acute gastroenteritis, Meckel’s diverticulum
School-age
-Acute GE, constipation, Sickle cell
Young males
-Crohn’s, UC, epididymitis
Young females
-Crohn’s, PID, ovarian cysts, UTI, pregnancy
Older adults
-Malignancies of GI and GU
-Diverticulitis
-Perforated ulcers
-Cholecystitis
Investigations:(Laboratory, Imaging, & special)
Lab:
-CBC, Hb,DLC for infection, anemia.
-HCG assy for pregnancy.
-Electrolytes :
K.
Na.
Bicarbonate HCO3.
-Amylase for pancreatitis.
-Liver function test:
-PT(Prothrombin time), PTT(Partial thromboplastin time).
-Alkaline phosphatase.
-ALT, AST.
-Urinalysis.
-Glucose in blood & urine.
Imaging:
-Plane abdominal x-ray (showing obstruction, calcification, uretric calculi, air, fluids.
-Ultrasound shows almost all the abdominal pathology.
-CT Scan.
-MRI specially in pregnant females.
Special tests:
-HbA1C in DM.
-Gastrointestinal Tract Endoscopy.
-Hb Electrophoresis in SCD.
-Others. As ECG.
Treatment:
Medical treatment:
-Analgesic drugs.
-Hydration , and IV nutrition for electrolytes disturbance.
-Antibiotics.
-Others depend on the diagnosis.
Causes that are always treated medically:
Myocardial infarcts, Acute pericarditis
PN, pulmonary infarction
GE reflux, hepatitis
DKA, Ac Adrenal Insufficiency
Acute Porphyria
Rectus muscle hematoma
Pyelonephritis, Acute salpingitis
Sickle cell crisis
Surgical treatment:
-Appendectomy.
-Cholecystectomy.
-Laparoscopy.
-others.
References:
1-Medscape article of Acute abdomen, & acute appendicitis in:
http://emedicine.medscape.com/article/195976-print (SIGN IN 6-8-2010)

th
2-Harrison’s principles & practice of medicine 17 ed 2008 CH: 14 abdominal pain.
th
3-Baily & Love’s short practice of surgery 25 ED.
th
4-Schwartz’s principles & practice of surgery 9 ED 2009 CH: 30 The appendix.
ACUTE APPENDICITIS
Introduction:
Appendicitis is a common and urgent surgical illness with manifestations, associated with generous overlap with other
clinical syndromes, and significant morbidity, which increases with diagnostic delay. No single sign, symptom, or
diagnostic test accurately confirms the diagnosis of appendiceal inflammation in all cases.
Important points in surgical view of the appendix:
1. Appendectomy for appendicitis is the most commonly performed emergency operation in the world.
2. Despite the increased use of ultrasonography, computed tomographic scanning, and laparoscopy, the rate of misdiagnosis of
appendicitis has remained constant (15.3%), as has the rate of appendiceal rupture. The percentage of misdiagnosed cases of
appendicitis is significantly higher among women than among men.
3. Appendicitis is a polymicrobial infection, with some series reporting up to 14 different organisms cultured in patients with
perforation. The principal organisms seen in the normal appendix, in acute appendicitis, and in perforated appendicitis are
Escherichia coli and Bacteroides fragilis.
4. Antibiotic prophylaxis is effective in the prevention of postoperative wound infection and intra-abdominal abscess. Antibiotic
coverage is limited to 24 to 48 hours in cases of nonperforated appendicitis. For perforated appendicitis, 7 to 10 days of
treatment is recommended.
5. Compared with younger patients, elderly patients with appendicitis often pose a more difficult diagnostic problem because of
the atypical presentation, expanded differential diagnosis, and communication difficulty. These factors contribute to the
disproportionately high perforation rate seen in the elderly.
6. The overall incidence of fetal loss after appendectomy is 4% and the risk of early delivery is 7%. Rates of fetal loss are
considerably higher in women with complex appendicitis than in those with negative appendectomy and those with simple
appendicitis. Removing a normal appendix is associated with a 4% risk of fetal loss and 10% risk of early delivery.
7. Recent data on appendiceal malignancies from the Surveillance, Epidemiology, and End Results program identified mucinous
adenocarcinoma as the most frequent histologic diagnosis, followed by adenocarcinoma, carcinoid, goblet cell carcinoma, and
signet-ring cell carcinoma.
8-Fever is an important sign in any suspected surgical abdomen.
Anatomy:
-It is a worm shape small tube only found in humans that contains large amount of lymphoid tissue as around the hole
gastrointestinal tract which is mainly needed in the early development for gaining immunity but in old age it is not so
important.
-Length 7-13 cm
-Covered by a fold of peritoneum called mesoappendix
-It is attached to the posteriomedial surface of the cecum about 1 inch below the illiocecal junction which is called
McBurney’s point.
-McBurney’s point can be located by surface anatomy as a point which divide the line between the umbilicus & the
anterior superior iliac spine in to 1/3 near to the spine & 2/3 near to the umbilicus.
-Appendix is supplied by the appendicular artery which is a branch of the superior mesenteric artery.
-Lymphatic drainage is through mesenteric nodes to the ciliac group of lymph nodes.
- The base of the appendix is easily identified by the teniae coli at the point of convergence.
-Positions of the tip of the appendix is variable these positions include:

-Retrocecal a round 75%.
-Pelvic 21%.
-Post ilial 5%.
-Subcecal 1.5%.
-Nerve supply sympathetic & parasympathetic is through vagus nerve, superior mesenteric nerve supply sensations
th
which is carried by the 10 thoracic nerve which explain the referred pain.
Pathophysiology:
Obstruction of the appendiceal lumen leads to distension of the appendix due to accumulated intraluminal fluid.
Ineffective lymphatic and venous drainage allows bacterial invasion of the appendiceal wall, edema formation,
and, in advanced cases, perforation and abscess formation with pus production into the peritoneal cavity causing
peritoneal irritation. This occur mainly by:
-Feces.
-Lymphoid follicular hyperplasia.
Epidemiology:
Incidence of appendicitis is lower in cultures with a higher intake of dietary fiber. Dietary fiber is thought to decrease
the viscosity of feces, decrease bowel transit time, and discourage formation of fecaliths, which predispose individuals
to obstructions of the appendiceal lumen.
The lifetime rate of appendectomy is 12% for men and 25% for women, with approximately 7% of all people
undergoing appendectomy for acute appendicitis during their lifetime.
Morbidity & Mortality:
 The overall mortality rate of 0.2-0.8% is due to complications of the disease rather than to surgical
intervention.
 Mortality rate rises above 20% in patients older than 70 years, because of diagnostic and therapeutic delay.
 Perforation rate is higher among patients younger than 18 years and patients older than 50 years, possibly
because of delays in diagnosis. Appendiceal perforation is associated with a sharp increase in morbidity and
mortality rates.
Sex: M/FM
1.4/1
Age:
 Incidence of appendicitis gradually rises from birth, peaks in the late teen years, and gradually declines in
the geriatric years. The median age at appendectomy is 22 years.
 Although rare, neonatal and even prenatal appendicitis have been reported.
History:
 Variations in the position of the appendix, age of the patient, and degree of inflammation make the clinical
presentation of appendicitis notoriously inconsistent.
 A retrocecal appendix may cause principally flank or back pain; a pelvic appendix, principally suprapubic
pain; and a retroileal appendix, testicular pain, presumably from irritation of the spermatic artery and ureter.
Intestinal malrotation also is responsible for puzzling pain patterns.
 It is important to remember that the position of the appendix is variable. Of 100 patients undergoing 3-D
multidetector CT, the base of the appendix was located at McBurney's point in only 4% of patients. In 36% of
patients, the base was within 3 cm of McBurney's point; in 28%, it was 3-5 cm from McBurney's point; and, in
36% of patients, the base of the appendix was more than 5 cm from McBurney's point.
 Many other disorders present with symptoms similar to those of appendicitis which should be differentiated
clinicaly. These include the following:
o Pelvic inflammatory disease (PID) or tubo-ovarian abscess
o Endometriosis
o Ovarian cyst or torsion
o Ureterolithiasis and renal colic
o Degenerating uterine leiomyomata
o Diverticulitis
o Crohn disease
o Colonic carcinoma
o Rectus sheath hematoma
o Cholecystitis
o Bacterial enteritis
o Mesenteric adenitis
o Omental torsion
 Classic history of anorexia and periumbilical pain followed by nausea, right lower quadrant (RLQ) pain,
and vomiting occurs in only 50% of cases.
 When vomiting occurs, it nearly always follows the onset of pain. Vomiting that precedes pain is
suggestive of intestinal obstruction, and the diagnosis of appendicitis should be reconsidered.
 Nausea is present in 61-92% of patients; anorexia is present in 74-78% of patients.
 Diarrhea or constipation is noted in as many as 18% of patients.
 Anorexia is nearly always accompanies appendicitis.
 Duration of symptoms is less than 48 hours in approximately 80% of adults but tends to be longer in elderly
persons and in those with perforation. Approximately 2% of patients report duration of pain in excess of 2
weeks.
 A history of similar pain is reported in as many as 23% of cases.
 An inflamed appendix near the urinary bladder or ureter can cause irritative voiding symptoms and hematuria
or pyuria. Cystitis in male patients is rare in the absence of instrumentation. Consider the possibility of an
inflamed pelvic appendix in male patients with apparent cystitis.
 Also consider the possibility of appendicitis in pediatric or adult patients who present with acute
urinary retention.
 RLQ tenderness is present in 96% of patients, but this is a nonspecific finding. Rarely, left lower quadrant
(LLQ) tenderness has been the major manifestation in patients with situs inversus (Congenital anomaly) or in
patients with a lengthy appendix that extends into the LLQ.
 Low grade fever 37.2-38 C.
 The most specific physical findings are rebound tenderness, pain on percussion, rigidity, and guarding.
 The Rovsing sign (RLQ pain with palpation of the LLQ) suggests peritoneal irritation in the right lower
quadrant precipitated by palpation at a remote location.
 The obturator sign (RLQ pain with internal and external rotation of the flexed right hip) suggests that the
inflamed appendix is located deep in the right hemipelvis.
 The psoas sign (RLQ pain with extension of the right hip or with flexion of the right hip against resistance)
suggests that an inflamed appendix is located along the course of the right psoas muscle.
 These signs are present in a minority of patients with acute appendicitis so absence do not role out
appendicitis.
 Dunphy's sign (sharp pain in the RLQ elicited by a voluntary cough) may be helpful in making the clinical
diagnosis of localized peritonitis. Similarly, RLQ pain in response to percussion of a remote quadrant of the
abdomen, or to firm percussion of the patient's heel, suggests peritoneal inflammation.
 The Markle sign, pain elicited in a certain area of the abdomen when the standing patient drops from
standing on toes to the heels with a jarring landing, was studied in 190 patients undergoing appendectomy
and found to have a sensitivity of 74%.
 Male infants and children occasionally present with an inflamed hemiscrotum due to migration of an inflamed
appendix or pus through a patent processus vaginalis. This is often initially misdiagnosed as acute testicular
torsion.
Causes:
 Obstruction of the appendiceal lumen due to:

o Fecaliths form when calcium salts and fecal debris become layered around a nidus of inspissated
fecal material located within the appendix.
o Lymphoid hyperplasia is associated with a variety of inflammatory and infectious disorders including
Crohn disease, gastroenteritis, amebiasis, respiratory infections, measles, and mononucleosis.
o Obstruction of the appendiceal lumen has less commonly been associated with parasites (eg,
Schistosomes species, Strongyloides species), foreign material (eg, shotgun pellet, intrauterine
device, tongue stud, activated charcoal), tuberculosis, and tumors.
Common Organisms Seen in Patients with Acute Appendicitis
Aerobic and Facultative Anaerobic

Gram-negative bacilli Gram-negative bacilli
Escherichia coli Bacteroides fragilis
Pseudomonas aeruginosa Other Bacteroides species
Klebsiella species Fusobacterium species
Gram-positive cocci Gram-positive cocci
Streptococcus anginosus Peptostreptococcus species
Other Streptococcus species Gram-positive bacilli
Enterococcus species Clostridium species
Differential Diagnosis:
-Abdominal Abscess. -Mesenteric Lymphadenitis.

-Cholecystitis and Biliary Colic. -Omental Torsion.
-Constipation. -Ovarian Cysts.
-Crohn Disease. -Ovarian Torsion.
-Diverticular Disease. -Pediatrics, Intussusception.
-Ectopic Pregnancy. -Pelvic Inflammatory Disease.
-Endometriosis. -Renal Calculi.
-Gastroenteritis. -Spider Envenomations, Widow.
-Gastroenteritis, Bacterial. -Urinary Tract Infection.
-Inflammatory Bowel Disease.
-Meckel Diverticulum.
-Mesenteric Ischemia.
Investigations:(Laboratory, Imaging, & Special)
Laboratory:
-Full Blood Count (FBC),WBC,& DLC for leukocytosis (more than 11,000 cells/cm) specially neutrophils more than
75%.
-C-reactive protein: (CRP) is an acute-phase reactant synthesized by the liver in response to infection or
inflammation.
-ESR (Erythrocyte sedimentation rate) to role out all the chronic disease.
- Urinalysis specially when there is some urinary symptoms.
-Human chorionic gonadotropic assay for pregnancy.
Imaging:
- Abdominal CT has become the most important imaging study in the evaluation of patients with atypical
presentations of appendicitis.
Advantages of CT scanning include its superior sensitivity and accuracy compared with those of other imaging
techniques, ready availability, noninvasiveness, and potential to reveal alternative diagnoses. Disadvantages include
radiation exposure, potential for anaphylactic reaction if intravenous contrast agent is used, lengthy acquisition time if
oral contrast is used, and patient discomfort if rectal contrast is used.
- Ultrasonography.
Advantages of sonography include its noninvasiveness, short acquisition time, lack of radiation exposure, and
potential for diagnosis of other causes of abdominal pain, particularly in the subset of women of childbearing age.
Many authorities believe that ultrasonography should be the initial imaging test in pregnant women and in pediatric
patients because radiation exposure is particularly undesirable in these groups.
- Abdominal radiography x-ray.
- Magnetic resonance imaging.
Treatment:
-Hydration.
-Analgesics.
-Antibiotics.
-Antiemitics.
-Appendectomy:
Conventional appendectomy.
Types of incision:
Gridiron incision.
Lanz incision.
Rutherford Morison incision.
Laparoscopic appendectomy.
Complications:
Complications of appendicitis may include the following:
Presurgery:
-Perforation.
Patients at risk of perforation:
-Anasthesia irritation.
-Abdominal/pelvic abscess
-Appendicular mass (Management is by using conservative treatment as Ochsner-Sherren regimen) which prevent
surgery.
Intrasurgical:
-Hemorrhage.
-Infection.
Postsurgical:
-Wound infection
-Incisional hernia.
- Bowel obstruction
-Abdominal/pelvic abscess
-Respiratory pneumonitis.
-Venous thrombosis & embolism.
-Faecal fistula.
-Pylephlebitis.
Stump appendicitis - Although rare, approximately 36 reported cases of appendicitis in the surgical stump after prior
appendectomy exist.
Death (rare)
Prognosis :
Almost all the patient have excellent prognosis.
Perforation and abscess formation are more likely to occur in pregnant patients with appendicitis than in nonpregnant
patients with appendicitis.
References:
-Medscape resource website.
th
-Baily& Love’s Short practice of surgery 25 ED, CH: 67 The vermiform appendix,P:1204-1219.
GOITER
ANATOMY, PHYSIOLOGY,PATHOPHYSIOLOGY,
EVALUATION,& MANAGEMENT
GROUP: B3
SUPERVISIED BY: Dr.OSSAMA ZAKARIA

THYROID GLAND
Embryology:
The thyroid gland arises as an outpouching of the primitive foregut around the third week of gestation. It originates
at the base of the tongue at the foramen cecum. Endoderm cells in the floor of the pharyngeal pouch thicken to form
the medial thyroid lobe that descends in the neck anterior to structures that form the hyoid bone and larynx. During
its descent, it remains connected to the foramen cecum via an epithelial-lined tube known as the thyroglossal duct.
The epithelial cells give rise to the thyroid follicular cells. The lateral lobe is derived from the fourth branchial pouch
neuroectodermal in origin (ultimobranchial bodies) which leads to formation of the thyroid C cells (Thyrocalcetonin),
or parafollicular cells. Both lobes fused together at fifth week of gestation. Thyroid follicles are initially apparent by 8
weeks, and colloid formation begins by the eleventh week of gestation.
Congenital anomalies:
-Thyroglossal Duct Cyst and Sinus : the most commonly encountered congenital cervical anomalies. During the fifth
week of gestation, the thyroglossal duct lumen starts to obliterate, and the duct disappears by the eighth week of
gestation.
-Lingual Thyroid: It represents a failure of the median thyroid lobe to descend normally and may be the only thyroid
tissue present. Intervention becomes necessary for obstructive symptoms such as choking, dysphagia, airway
obstruction, or hemorrhage. Many of these patients develop hypothyroidism. Selective treatment is Suppression of
TSH.
-Ectopic Thyroid.
-Pyramidal Lobe: Normally the thyroglossal duct atrophies, although it may remain as a fibrous band. In
about 50% of individuals, the distal end that connects to the thyroid persists as a pyramidal lobe projecting
up from the isthmus, lying just to the left or right of the midline.
Anatomy:
The adult thyroid gland is brown in color and firm in consistency, located in the midline of the neck below the
thyroid cartilage, & posterior to the strap muscles . It weighs approximately 20 g, but gland weight varies with body
weight and iodine intake. It is connected in the midline by an isthmus that is located just inferior to the cricoid
cartilage. A pyramidal lobe is present in about 50% of patients. The thyroid lobes extend to the midthyroid cartilage
superiorly and lie adjacent to the carotid sheaths and sternocleidomastoid muscles laterally. The strap muscles
(sternohyoid, sternothyroid, and superior belly of the omohyoid) are located anteriorly and are innervated by the
ansa cervicalis (ansa hypoglossi). The thyroid gland is enveloped by a loosely connecting fascia that is formed from
the partition of the deep cervical fascia into anterior and posterior divisions. The true capsule of the thyroid is a thin,
densely adherent fibrous layer that sends out septa that invaginate into the gland, forming pseudolobules. The
thyroid capsule is condensed into the posterior suspensory or Berry's ligament near the cricoid cartilage and upper
tracheal rings. A long the posterior surface four parathyroid glands are there.
Blood Supply:
-Superior thyroid artery from external carotid artery divide into anterior and posterior branches at the apices of the
thyroid lobes.
-Inferior thyroid artery from the thyrocervical trunk.
-Thyroidea Ima artery.
-Innominate artery in 1 to 4% of individuals arising directly from the aorta supplying the isthmus.
Notes:
-The inferior thyroid artery crosses the recurrent laryngeal nerve (RLN), necessitating identification of the RLN before
the arterial branches can be ligated in thyroid operation.
-The venous drainage of the thyroid gland occurs via multiple small surface veins which coalesce to form three sets
of veins:
-Superior thyroid vein.
-Middle thyroid vein.
-Inferior thyroid vein.
Superior & middle drain in to internal jugular vein, while The inferior vein often form a plexus, which drains into the
brachiocephalic veins.
Nerves:
-The left recurrent laryngeal nerve (RLN) arises from the vagus nerve & crosses the aortic arch, loops around the ligamentum
arteriosum, and ascends medially in the neck within the tracheoesophageal groove.
-The right RLN arises from the vagus at its crossing with the right subclavian artery.
-The RLNs innervate all the intrinsic muscles of the larynx, except the cricothyroid muscles, which are innervated by the external
laryngeal nerves. Injury to one RLN leads to paralysis of the ipsilateral vocal cord. Bilateral injury leads to airway obstruction,
necessitating emergency tracheostomy, or loss of voice.
-Sympathetic innervation of the thyroid gland is provided by fibers from the superior and middle cervical sympathetic ganglia.
The fibers enter the gland with the blood vessels and are vasomotor in action. Parasympathetic fibers are derived from the vagus
nerve and reach the gland via branches of the laryngeal nerves.
Lymphatic drainage:
Thyroid gland is associated with extensive lymphatic network. Intraglandular lymphatic vessels connect both thyroid lobes
through the isthmus and also drain to perithyroidal structures and lymph nodes. Thyroid cancers may metastasize to any region in
the neck. See figure B describing the classification of lymph nodes in the neck according to level of metastatic involvement.
Histology:
Microscopically, the thyroid is divided into lobules that contain 20 to 40 follicles. There are about 3 x 106 follicles in the adult
male thyroid gland. Each follicle is lined by cuboidal epithelial cells and contains a central store of colloid secreted from the
epithelial cells under the influence of the pituitary hormone TSH.
Physiology:
Synthesis of thyroid hormones(T3,T4, & Calcitonin):
-Thyroxine:
The four basic steps for formation of thyroid hormone:
-Trapping of inorganic iodide from the blood.
-Oxidation of iodide to iodine.
-Binding of iodine with tyrosine to form iodotyrosines.
-Coupling of mono-iodotyrosines and di-iodotyrosine to form T3, T4
Note: The metabolic effects of the thyroid hormones are due to unbound T4 and T3 (0.03% and 0.3% of the total
circulating hormones respectively).
Activity time in T4 is 4-14 days while T3 within few hours.
-Calcitonin:
Parafollicular C cells are neuroendocrine in origin which is important in maintenance of blood Ca level. It is also used as a
marker for thyroid medullary carcinoma.
Hypothalamic-Pitutary-Thyroid axis:
The hypothalamus produces a peptide, the thyrotropin-releasing hormone (TRH), which stimulates the pituitary to release TSH or
thyrotropin. TRH reaches the pituitary via the portovenous circulation. TSH, a 28-kDa glycopeptide, mediates iodide trapping,
secretion, and release of thyroid hormones, in addition to increasing the cellularity and vascularity of the thyroid gland. The TSH
receptor (TSH-R) belongs to a family of G-protein coupled receptors that have seven transmembrane-spanning domains and use
cyclic adenosine monophosphate in the signal-transduction pathway. TSH secretion by the anterior pituitary is also regulated via a
negative feedback loop by T4 and T 3. Because the pituitary has the ability to convert T4 to T3, the latter is thought to be more
important in this feedback control. T 3 also inhibits the release of TRH.
Thyroid stimulating antibodies:
A family of IgG immunoglobulin bind with TSH receptors and activate thyroid follicular cells this is usually responsible with
cases of thyrotoxicosis with serum TSH very low, and T3,T4 is high.
Therapeutic notes: T3,T4 are used as a suppressive goal, while recombinant TSH is used with radiation therapy to maximize
iodine uptake as an alternative to thyroid hormone withdrawal.
Thyroid hormone Functions:
Free thyroid hormone enters the cell membrane by diffusion or by specific carriers and is carried to the nuclear membrane by
binding to specific proteins. T4 is deiodinated to T 3 and enters the nucleus via active transport, where it binds to the thyroid
hormone receptor. The T3 receptor is similar to the nuclear receptors for glucocorticoids, mineralocorticoids, estrogens, vitamin D,
and retinoic acid. In humans, two types of T 3 receptor genes ( and ) are located on chromosomes 3 and 17. Thyroid receptor
expression depends upon peripheral concentrations of thyroid hormones and is tissue specific—the form is abundant in the central
nervous system, whereas the form predominates in the liver. Each gene product has a ligand-independent, amino-terminal domain;
a ligand-binding, carboxy-terminal domain; and centrally located DNA-binding regions. Binding of thyroid hormone leads to the
transcription and translation of specific hormone responsive genes.
Thyroid hormones affect almost every system in the body. They are important for fetal brain development and skeletal
maturation. T3 increases oxygen consumption, basal metabolic rate, and heat production by stimulation of Na+/K+ ATPase in
various tissues. It also has positive inotropic and chronotropic effects on the heart by increasing transcription of the Ca 2+
ATPase in the sarcoplasmic reticulum and increasing levels of beta-adrenergic receptors and concentration of G proteins.
Myocardial alpha receptors are decreased and actions of catecholamines are amplified. Thyroid hormones are responsible for
maintaining the normal hypoxic and hypercapnic drive in the respiratory center of the brain. They also increase GI motility,
leading to diarrhea in hyperthyroidism and constipation in hypothyroidism. Thyroid hormones also increase bone and protein
turnover and the speed of muscle contraction and relaxation. They also increase glycogenolysis, hepatic gluconeogenesis,
intestinal glucose absorption, and cholesterol synthesis and degradation.
GOITER
Definition:
Goiter (from the Latin guttur, throat), defined as an enlargement of the thyroid, have been recognized since 2700 B.C.
even though the thyroid gland was not documented as such until the Renaissance period.
Pathophysiology:
-Physiological Iodine deficiency leads to hyperplasia of the gland in order to compensate low T3,T4.
-Inflammation such as thyroiditis.
-Autoimmune such as hashimoto’s thyroiditis.
-Neoplastic either benign, or malignant (Adenoma, & thyroid carcinoma respectively).
-Others such as amyloidosis.
Classification of thyroid swellings:
1-Simple goiter (euthyroid, non toxic)
Diffuse hyperplastic
Physiological
Pubertal
Pregnancy
Multinodular goiter
2-Toxic
Diffuse
Graves’ disease
Multinodular goiter
Adenoma
3-Neoplastic
Benign
Adenoma
Malignant
Follicular carcinoma
Anaplastic carcinoma
Medullary carcinoma
Papillary carcinoma
4-Inflammatory
Autoimmune
Chronic lymphocytic thyroiditis
Hashimoto’s thyroiditis
Granulomatous
De Quervain’s thyroiditis
Fibrosing
Riedel’s thyroiditis
Infection
Acute (bacterial thyroiditis, viral thyroiditis,& subacute thyroiditis)
Chronic (tuberculous, or syphilitic)
Others
Amyloid
Causes:
1- physiological: puberty & pregnancy.

2- Iodine deficient (endemic)
3- Hyperthyroidism (Grave's disease)
4- Adenomatus (nodular) goiter
5- Thyroiditis (Hashimoto's, De Quervain's thyroditis, Riedel's thyroditis)
6- Thyroid malignancy.
7- Ingestion of goitrogens (excessive iodine, phenylbutazone, lithium)
8-Dyshormonogenesis.
Clinical Evaluation of Patient with thyroid disease:
History:
1- Lump or swelling in the neck so detailed history about the swelling is important.
2- Discomfort during swallowing or dysphagia.
3- Dyspnea: due to deviation or compression of the trachea..
4- painfull or painless (Painfull in cases of thyroiditis, & usually painless suggests malignancy)
5- hoarsness: it might be caused by paralysis of one recurrent laryngeal nerve ( i.e. the lump is a neoplastic
Carcinoma invading the nerve).
6-Sweating, weight loss, fever, or weight gain, & coldness.
7-History of neck radiation.
8-History of cough, hemoptysis after swelling in the neck suggests metastasis to the lung.
9-Neurological symptoms.
Examination:
Local neck examination:
Inspection:
1- Ask to swallow all thyroid swelling ascend during swallowing
2- Ask to protrude the tongue if the lump moves up, it's thyroglossal cyst
3- Look for the position of thyroid cartilage, is it in the center Or deviated laterally
4- Look if there is distended veins, it indicates retrosternal extenstion.
5-Ask the patient to open his mouth to see if there is any abnormalities.
6-Look for the swelling if there is any visible pulsations.
Palpation:
From front:
1- Position of trachea
2- Thyroid cartilage
3-Thrill.
From behind:
1- Ask the patient to swallow to confirm if is a thyroid swelling.
2- Describe it (size, Shape, surface, consistency, mobility) & thrill if present.
3- Palpate the whole groups of neck lymph nodes for tenderness, temperature, & swelling.
Percussion:
Percuss along the clavical & over the sternum & upper chest wall to see if there is any extension below suprasternal
notch
( Retrosternal thyroid extension).
Auscultation:
A systolic bruit may be heared over each lobe.
Examination of the eye:
Inspect the eye for associated exophthalmus, lid lag, lid retraction, ophthalmoplagia, & chemosis.
Examination of CVS:
Look for palpitation, tachycardia, or bradycardia & hypotension.
General Examination:
Weakness, tiredness, limb sweating,
Investigations:
Laboratory:
1- Free T3 (3–9 pmol/L) & T4 (Reference Range 12–28 pmol/L) :

T4 level will usually establish whether the gland is over active or not, but if the clinical state is hyperactivity & T4 is
normal, then T3 should be done.
2-Total T3 (Reference Range 1.5–3.5 nmol/L) & T4 (Reference Range 55–150 nmol/L) :
Total T4 levels reflect the output from the thyroid gland, whereas T 3 levels in the nonstimulated thyroid gland are more indicative
of peripheral thyroid hormone metabolism, and are, therefore, not generally suitable as a general screening test. Total T 4 levels are
increased not only in hyperthyroid patients, but also in those with elevated Tg levels secondary to pregnancy,
estrogen/progesterone use, or congenital diseases. Similarly, total T 4 levels decrease in hypothyroidism and in patients with
decreased Tg levels due to anabolic steroid use and protein-losing disorders like nephrotic syndrome. Individuals with these latter
disorders may be euthyroid if their free T 4 levels are normal. Measurement of total T 3 levels is important in clinically hyperthyroid
patients with normal T4 levels, who may have T3 thyrotoxicosis. As discussed previously in Thyroid Hormone Synthesis,
Secretion, and Transport, total T3 levels often are increased in early hypothyroidism.
3- TSH : (Normal 0.5–5 U/mL) for pituitary function.
Raised in hypothyroidism & low in hyperthyroidism .
4-TRH for the function of hypothalamus.
5- serum LATS:
The presence of LATS is diagnostic of Grave's
LATS: long acting thyroid stimulating factor, it is an IgG & they activate TSH receptors on follicular membrane &
has much longer …. In circulation than TSH
6- Thyroid antibodies:
Like antithyrogobulin & antimitochondrial Ab are ↑↑ in Hashimoto's thyroiditis
7- Serum Thyroglobulin.
8- Serum Calcitonin (0–4 pg/mL Basal): Used as a selective marker for medullary thyroid carcinoma.
Imaging:
1-Radionuclide Imaging: By I131 or technetium 99 .The injected isotope is taken by thyroid gland & distributed
uniformly in a normal thyroid. A nodule in the thyroid gland that is hyperactive so-called (hot nodule). A nodule that
is not producing T4 will not take up the isotope so called (cold nodule) & it indicates a cyst or tumor.
2-Neck Ultrasound:
-To know if the lump is cystic or solid

-To know the general shape & outline of the gland.
-To assess for cervical lymphadenopathy
-To guide for biopsy.
3-Computed tomography (CT scan), & MRI:
- Evaluating the extent of large, fixed, or substernal goiters (which cannot be evaluated by ultrasound) and their
relationship to the airway and vascular structures.
4-Plane chest X-ray for tracheal displacement & compression.
5-Fine needle aspiration cytology (FNAC).
6-Tissue biopsy.
7-ECG for changes in hyperthyroidism & hypothyroidism such as atrial fibrillation..
8- Laryngoscopy: used preoperative to determine the mobility of the vocal cords. Used also for medico-legal aspect.
Clinical Presentation:
Euthyroidism
Causes:
1- physiological ( puberty, pregnancy)
2- iodine deficiency (Endemic goiter)
Hypothyroidism
Causes:
1- with a goiter:
- Chronic lymphocytic thyroditis ( Hashimoto's)
- Drugs ( lithium)
- Iodine deficiency
2- without a goiter:
- Idiopathic atrophy
- Thyroidectomy
- After radioiodine therapy
- Thyroid agenesis
- Pituitary disease
- Hypothalamic disease
Signs:
1- In the neck:
Normal, or enlarged Thyroid
2- In the eyes:
the eye is normal
swelling
the eye lids becomes swollen & heavy
→ periorbital puffness Euthyroid Hyperthyroid as Hypothyroid
→the hair of the lateral third of the
eyebrows fall down thyrotoxicosis
3- General signs:
- In white skinned patient, the skin is smooth & pale while the cheeks are often slightly flushes
- Patient is overweight with excessive connective tissue & fat in supraclavicular fossa, across the back of the neck &
over the shoulders
- the hair looks thin & fall out.
- the skin is dry & inelastic
- the hands are puffy & spade like
- the tongue is enlarged
- the voice becomes hoarse
4- CVS signs:
- bradycarida & hupotension: both will be reversed if heart failure develops
5- Neurological signs:
- retarded mental alterness & responding to questions
- slow movements (bradykinesis)
- slow recovery phase ankle jerk
- sluggish reflexes
Treatment:
Oral thyroxin (0.1- 0.2) as a single daily dose.
Hyperthyroidism
Causes:
1- Exogenous: excessive thyroid hormone ingestion
2- Pituitary: pituitary adenoma.
3- Thyroid: Grave's disease ( excessive stimulation of thyroid), subacute thyroiditis (excessive release of hormone)
4- Iodine load
5-Thyroid malignancy.
Clinical Signs:
1- In the neck:
thyrotoxicosis can be present without any enlargement of the gland.
Enlargement can be diffuse, nodular or tender depending on the cause
A diffusely enlarged hyperemic gland usually has a systolic bruit audible over the lobes
2-In the eyes:
A. lid retraction: due to overactivity of the involuntary part of levator palpebrae superioris muscle. The upper lid is
raised & lower lid is normal.
B. Lid lag: the upper eyelids lags behind the moving down eyeball while the head is fixed.
C. Exophthalmous: the eyeball is pushed forward by an increase in retro-orbital fat & cellular infiltration.
Sclera become visible all around the iris
Patient can look upward without wrinkling forehead ( Joffrey's sign)
Difficulties in conversion
If sever, patient can't close his eyelid & may have corneal ulcer
D. Ophalmoplegia:
Superior & lateral rectus + inferior oblique are the most affected muscles & they prevent the patient from looking
upwards & outwards.
E. Chemosis:
Edema of the conjuctiva
Due to obstruction of venous & lymphatic drainge of the conjuciva by the increase retro-orbital pressure.
3- metabolic signs:
patient looks thin & his face & hand may be wasted
patient may looks hot & sweating even in a cold room
4- CVS signs:
Tachycardia (persist during sleep)
Atrial fibrillation
If heart failure developed, ….at the base of the lung & ankle edema may develop.
5- Neurological signs:
Agitation & nervousness
Fine tremors
Treatment:
1- antithyroid:
a- carbimazole: patient should remain on a maintenance dose up to 2 years.
Side Effects: joint pain, skin rash, fever, agranulocytosis.
b- Propylthiocracil (300-600 mg/day)

c- Propranolol (symptomatic treatment)
2- Radioactive iodine:
I131 is given orally

It takes 8-12 weeks before patient becomes euthyroid so, antithyroid drugs are given during this period. It is
appropriate for middle age patient who failed with medical treatment & can't go to surgery.
Most of the patient will develop hypothyroidism later on
It is contraindicated in pregnancy & childhood.
3- Surgery:
Indications:
1- Failure of medical treatment
2- Drug sensitivity in young patient.
3- Large goiter with compression symptoms.
4- Malignancy
5-Recurrent cyst.
6-FNAC Positive
Preoperative preparation:
-Patient should become euthyroid before surgery to prevent thyroid crisis
-Assesment of vocal cords condition.
Operations:
Solitary benign nodule (lobectomy).
Cancers:
-Papilary carcinoma needs total thyroidectomy & cervical lymph node resection (Transmitted mainly via lymphatics).
-Folicullar carcinoma needs hemithyroidectomy if complicated thyroidectomy (Transmitted via blood).
-Medullary carcinoma needs total thyroidectomy(Transmitted via blood).
-Anaplastic carcinoma no need for thyroidectomy because the cancer has already metastasize at the time of diagnosis.
Thyrotoxicosis → subtotal thyroidectomy.
Complications:
Pre operation:
-Side effect of anesthesia.
Intra operation:
-Hemorrhage.
- thyroid storm:
patient will have pyrexia, agitation, excessive sweating & extreme tachycardia & atrial fibrillation
treated by rapid administration of:
1- antithyroid drugs
2- IVF
3- Cooling for pyrexia
4- Barbiturates
5- Digoxin
6-wound infection.
7- Recurrent thyrotoxicosis.
8- Keloid scar.
Post operation:
- hemorrhage:
-recurrent laryngeal nerve damage:
If unilateral→ hoarseness
If bilateral→ airway obstruction & emergency tracheostomy is required
- superior laryngeal nerve damage:
Lead to loss of high pitch & inability to make explain sounds
Usually transient
- hypoparathyroidism:
may lead to tetani
present within the first week of surgery
manifested by tingling sensation & corpopedal spasm
relieved by injection of Ca
- hypothyroidism:
In 15% of cases
Treated by hormonal replacement therapy .
Short notes about Examination of Thyrotoxicosis patient:
1.general appearance..
- Weight. loss. – anxiety.
-Restless. – sweating.
2.hands..
-Pulse(tachycardia, bounding/collapsing pulse, atrial fibrillation).
-Moisture. – fine tremor.
-Palmar erythema. – onycholysis.
-Warmth. – clubbing (thyroid acropathy).
3.arms..
-Proximal myopathy. - exaggerated reflexes.
4.eyes..
-Lid retraction. – lid lag.
-Exophthalmus(pt looks upward without wrinkling /difficult converging).
-Ophthalmoplegia. – chemosis.
5.chest..
-Gynecomastia. – murmur. -signs of CHF.
6.abdomen..
-Splenomegally.
7.legs..
- Pretibial myxoedema: red, thickened swelling above the lateral malleoli, which progress to thickened non pitting
edema of the feet.
Test for proximal myopathy & hyper reflexia in the legs.
8.Neck..
Inspection:
-Swelling.
-Movement of the swelling(tongue protrusion/swallowing).
-Scars of surgery. -pemberton’s sign.
Palpation:
-The gland(site, size, shape, surface, tenderness, temperature, thrill, consistency, relation to surrounding tissue)
-Lymph nodes. – tracheal deviation. -carotid arteries.
Percussion:
- Retrosternal extension.
Auscultation:
- Bruit over the thyroid &carotid arteries.
Reference:
1-Shwartz’s principles & practice of surgery 9th ED MC Graw Hill publishing company 2009 CH: 38. Thyroid,
Parathyroid, and Adrenal.
2-Bailey & Love’s Short practice of surgery 25th ED, Hodder Arnold publishing company CH:48 The
thyroid & Parathyroid Glands.
1-Stedman's Medical Dictionary, 27th Edition

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SURGERY (I) LOG BOOK

KING FAISAL UNIVERSITY

COLLEGE OF MEDICINE IN AL-AHSSA

-Summary of the Log Book.

-CASES (PRESENTED & NON-PRESENTED) In all weeks.

-BEDSIDE TEACHINGS & KEYNOTES.

-ASSIGNMENTS & RESEARCHES.

LOG BOOK FOR HOSPITAL ROTATION

1. No. of Patients examined : 13

2. No. of case histories presented : 13

3. Ward Attendance : All attended

4. No. of assignments completed : All assignments

5. Lectures attended : All lectures

Name & Signature of faculty : Name & signature of student:

Qasim Hussain AL-Haleimi

KING FAISAL UNIVERSITY

NAME: QASIM HUSSAIN AL-HALEIMI

Supervised by Dr. Mohammad Atif Khan

Diagnosis: Sickle cell Anemia Vaso-occlusive Crisis.

Summery of the case:

Case# 2 Date: 25-05-2010 Tuesday

Summary of the case:

Case#3 Date: 25-05-2010 Tuesday

Diagnosis: Foot swelling.

Summary of the case:

Summary of the case:

Case#5 Date: 25-05-2010 Tuesday

Diagnosis: Sebaceous cyst.

Case#6 Date: 29-05-2010 Saturday

Analgesic & Antibiotics.

His parents have DM and HTN.

Case#7 Date: 30-05-2010 Sunday

Diagnosis: Abdominal pain under investigation

The patient is a known case of SCD since childhood.

No history of blood transfusion.

No previous hospitalization like this time.

Father & mother is SCD. Relatives.

Examination of the abdomen:

Mild splenomegaly around 2-3 cm below the costal margin.

KING FAISAL UNIVERSITY

NAME: QASIM HUSSAIN AL-HALEIMI

CASE # 1 Trauma in the Abdomen Date: 05-06-2010 Saturday

Diagnosis: Acute Abdomen

Summary of the case:

Ultrasound of the fetus & abdomen.

Presented Clinical Cases

Case#1 Acute abdomen Date: 05-06-2010 Saturday

Diagnosis: Crohn's disease.

Mesalazine, 400mg, 3 times/day

CNS: mild headache

CVS: chest pain, palpitation.

CASE# 2 Acute abdomen Date: 06-06-2010 Sunday

Summary of the case:

No chronic diseases, no any surgical interventions

Anti-allergic drug 2 tablet/day

Father and Mother have HTN and DM.

Living with his family

-Right iliac fossa tenderness.

KING FAISAL UNIVERSITY

NAME: QASIM HUSSAIN AL-HALEIMI

Admission on: 06-06-2010.

Diagnosis: Tisticular tumor, with epididmorchitis