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ALHT 401 Case Study Steve

This essay will discuss the scenario of Steve, a 54 year old male complaining of bilateral flank pain. It will identify the patients main presenting problem by eliminating any other possible causes, discuss the pathophysiological process of the provisional diagnosis and develop an appropriate pre-hospital management plan using the best current evidence based literature. It is important to correctly identify the patients chief complaint in order to assess, treat and manage correctly and efficiently. Steve has presented with bilateral flank pain. Flank pain has many causes ranging from renal calculi, urinary tract infection (UTI), abdominal aortic aneyurism (AAA), pyelonephritis, appendicitis and diverticulitis. It is important to carry out a differential diagnosis in order to rule out any life threatening causes. Although AAA, appendicitis and diverticulitis can all present with flank pain plus or minus nausea, vomiting and fever there are differentiating symptoms such as the presence of polyuria and dysuria that could rule these causes out. Renal calculi presents with severe, cyclical, radiating pain and hypertension (Sanders, 2010), all of which is absent in this case. So, after a thorough review of the patients associated signs, symptoms and history the provisional diagnosis has been identified as a lower UTI that has developed into possible pyelonephritis with query sepsis. This diagnosis has been given based on the presence of flank pain, polyuria, dysuria, tachycardia, hypotension, febrile, increase in blood glucose level and decreasing Glasgow coma score (GCS). A UTI results from a bacterial infection in the urinary tract. It is often said that UTIs begin in the lower urinary tract (e.g. the bladder or urethra) and if it remains untreated they may ascend to the upper urinary tract and result in pyelonephritis, or infected kidney (Sanders, 2010). Pyelonephritis can result from reflux of the infected urine from the bladder

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to the kidneys. Bethel (2012) states that if pyelonephritis is at its most severe it can result in life threatening illnesses such as sepsis, kidney failure, multisystem failure and death. Hence this case is a true medical emergency. The identification of septic Pyelonephritis as the main presenting problem has been based purely on a history and presenting signs and symptoms. In the pre-hospital setting it is difficult to diagnose the exact cause without the appropriate diagnostic equipment such as blood cultures and urinalysis. It is also difficult to treat in the absence of correct medications such as antibiotics, however particular symptoms such as increasing temperature, hypotension, tachycardia which is essentially the clinical manifestation of sepsis can be treated and the patient must be transported to hospital. Bethel (2012) recognises that recently the move has been to treat UTI and kidney infection patients out of hospital, however this case is complicated with the presence of sepsis and requires transport to hospital. Aitkin, Schorr and Kleinpell (2013) describe sepsis as the bodys systemic inflammatory response to infection. The body releases chemical mediators known as cytokines in response to the activation of white blood cells (Aitkin et al, 2013). It is this response that causes the physiological reaction of sepsis including vasodilation, leaky capillaries due to increased permeability and increased clot formation (Aitkin et al 2013). The effects of sepsis on the body are extensive and life threatening causing complications such as renal failure, disseminated intravascular coagulation (DIC), hypoperfusion of organs and pulmonary odema (Daniels and Nutbeam, 2010). Daniels and Nutbeam (2010) state that the cardiovascular effects of sepsis are evident early in the disease process. They also discuss that hypotension in sepsis results from vasodilation and relative hypovolemia caused

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by increased capillary permeability (Daniels and Nutbeam (2010). Changes in GCS may result from a decline in cerebral blood flow. According to Bones criteria for the recognition of severe sepsis Steve meets the criteria for severe sepsis with the exception of a white blood cell count as this cannot be performed in the prehospital setting (Daniels and Nutbeam, 2010). The patient is tachycardic with a heart rate above 90, he is febrile with a temperature above 38 degrees, his respiratory rate exceeds 20 breaths per minute and the decline in GCS is suggestive of possible organ failure or dysfunction. The outlined management plan is as follows: Request for MICA back up, oxygen administration, ECG monitoring, insertion of two large bore cannulas, pain relief, fluid resuscitation, anti emetic administration, removal of clothing, notification to receiving hospital, rapid transport, continuous monitoring and reassessment en route. The following paragraphs will detail the specifics and provide a rationale for each intervention. Steves presentation meets the criteria of Systemic Inflammatory Response Syndrome (SIRS) found in Ambulance Victoria Clinical Practice Guidelines (2011). According to Ambulance Victoria (2011) the treatment required for this patient is MICA backup and normal saline 20ml/kg to be run over 30 minutes. The rationale behind receiving MICA back up for Steve is based on the possibility of an inadequate response from the fluid replacement, the decline in GCS and possibility of overall patient deterioration. According to Langley and Langley (2012) if a patient is unresponsive to fluid replacement therapy they are considered to be in septic shock, a life threatening condition that requires an intensive care admission. MICA has their own guideline for this patient and with the possibility of Steves condition declining MICA is definitely warranted.

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Langley and Langley (2012) suggests that if there is any form of cognitive impairment then high flow oxygen should be applied as this poses a risk to the patients airway. Furthermore Robson et al (2009) discusses the increase in metabolic demand which inadvertently increases oxygen demand. Robson et al (2009) recommends using high flow oxygen via a non re-breathe mask with reservoir bag whilst maintaining SpO2 of above 94%. For these reasons 10L/min oxygen via a non re-breathe mask will be placed on Steve and his saturations will be monitored closely. An increase in respiratory rate is also indicative of acidosis in the septic patient. During respiratory acidosis there is a rise in potassium levels this increase can cause cardiac arrhythmias which is why ECG monitoring is crucial in the septic patient (Langley and Langley, 2012).Blood glucose monitoring is also an important part of sepsis management as it can increase the patients metabolic demand and is recommended that any loss is replaced (Langley and Langley, 2012). The insertion of two large bore cannulas (14guage) into th e patients left and right antecubital fossa. The size, location and amount have been chosen as the patient needs rapid fluid administration( based on pascals law), medication administration, anticipation for diagnostic testing such as blood cultures in hospital and likelihood of deterioration. Steve has an allergy to morphine so the next drug of choice is IV fentanyl. According to Ambulance Victoria (2011) Fentanyl can be administered 25-50mcg at five minute intervals. Given the age of the patient 25mcg increments five minutely with a maximum dose of 200mcg is appropriate. Fentanyl 100mcg/2ml should be diluted with 8ml normal saline making it up to 100mcg/10mls. This means the dose at each interval will be 25mcg/2.5ml.Vital signs should be checked five minutely before each subsequent

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administration. Steve was also experiencing bouts of nausea and vomiting. To help combat this 10mg/2ml of IV Maxalon can be administered. Fluid replacement is a highly recommended treatment for sepsis. It is evident in numerous amounts literature. Dellinger et al (2013) recognise that within the first 6 hours it is important to begin fluid resuscitation to maintain mean arterial pressure (MAP), central venous pressure and urine output. This study also found that there was a reduced mortality rate for those who received fluid resuscitation early (Dellinger et al, 2013). Aitkin et al (2013) also recognise fluid replacement as an important intervention in sepsis to improve haemodynamic stability. For these reason 20ml/kg will need to be administered over the first thirty minutes as indicated by Ambulance Victoria (2011). When administering fluids to septic patients it is important to ensure the patients chest remains clear. In sepsis capillaries increase in permeability which increases the risk of pulmonary oedema (Zhang et al, 2012). It has been noted that Steve has an unsteady gait. In order to safely load Steve the stretcher will need to be bought into the house if safe to do so, otherwise using the wheelchair to wheel the patient out to the stretcher and then load him into the truck. Steves increasingly high temperature poses the risk of organ failure that follows a persistently high temperature. It is important to cool the patient down by stripping him down into underwear and cover him with a sheet to maintain privacy and dignity. Pre hospital notification and rapid transport is important in decreasing the risk of morbidity and mortality as aggressive treatment can be initiated on arrival in emergency (Robson et al, 2009 and Boardman, 2009).

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The initial call out of an elderly patient with flank pain would have some clinicians questioning why an ambulance was called however after a thorough assessment it is evident that Steve was a true medical emergency. The main presenting problem was sepsis caused by an untreated UTI. The treatment of a UTI in the pre-hospital setting is not possible without the appropriate diagnostic equipment or medication. Steves presentation was complicated with the presence of sepsis, a medical emergency that can be treated in the pre-hospital setting and by doing so can improve patient outcome.

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References Aitkin, L., Schorr, C. A., & Kleinpell, R. (2013). IMPLICATIONS OF THE NEW INTERNATIONAL SEPSIS GUIDELINES FOR NURSING CARE. American Journal Of Critical Care, 22(3), 212-222. doi:10.4037/ajcc2013158 Ambulance Victoria. (2010). Clinical practice guidelines for ambulance and MICA paramedics. Melbourne: Ambulance Victoria.

Bethel, J. (2012). Acute pyelonephritis: risk factors, diagnosis and treatment. Nursing Standard, 27(5), 51-56. Boardman, S., Richmond, C., Robson, W., & Daniels, R. (2009). Prehospital management of a patient with severe sepsis. Journal Of Paramedic Practice, 1(5), 183-188. Daniels, R., Nutbeam, T. (2010). ABC of Sepsis. Retrieved from http://primo.unilinc.edu.au/primo_library/libweb/action/dlDisplay.do?vid=ACU&doc Id=aleph002048553 Dellinger., Levy, M., Rhodes, A., Annane, D., Gerlach, H., Opal, S., & Moreno, R. (2013). Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Critical Care Medicine, 41(2), 580-637. doi:10.1097/CCM.0b013e31827e83af Excellent sepsis management! Langley, M., & Langley, C. (2012). Adult sepsis in a pre-hospital environment. Journal Of Paramedic Practice, 4(5), 260-265

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Robson, W., Nutbeam, T., & Daniels, R. (2009). Sepsis: a need for prehospital intervention?. Emergency Medicine Journal, 26(7), 535-538. doi:10.1136/emj.2008.064469 Sanders, M. J. (2010). Mosbys paramedic textbook (3rded.). St Louis: Mosby.

Zhang, Z., Lu, B., Ni, H., Sheng, X., & Jin, N. (2012). Prediction of pulmonary edema by plasma protein levels in patients with sepsis. Journal Of Critical Care, 27(6), 623-629. doi:10.1016/j.jcrc.2012.08.007

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