Necrotizing_Faciitis

Mrs M, who had been receiving treatment from her General Practitioner for a weeping lower leg ulcer , was admitted to hospital on the 22/05/2010 following a marked deterioration in her general condition. She was quickly diagnosed with sepsis, secondary to a leg ulcer. The following case study will explore the predisposing factors, and disease process of sepsis as it pertains to Mrs M's past and present medical history, and the treatment used to manage this condition. This study will also examine and critically analyse the pathophysiology, as the progression of the disease evokes a neuro-hormonal- chemical response, and related the findings to the clinical assessments undertaken throughout the varying stages. Mrs M, a rather obese lady, 70 years of age, was brought onto the emergency department of a semi rural hospital by the metropolitan ambulance service. Mrs M had been receiving regular treatment from her General Partitioner (GP) for a weeping lower leg ulcer. On this particular visit , her GP noted a marked deterioration in her mental state, and energy levels. Further examination revealed that she had a temperature(T) of 39.2 C, blood pressure(BP) 68/40, irregular heart rate(HR) 115 beats/minute, and a Sa02 84%. She was also complaining of increased intensity of the pain in her leg, which when examined, appeared more oedematous and reddened than on previous visits. This lead the GP to call an ambulance Mrs M was an elderly lady, and although requiring minimal assistance from her husband with normal activities of daily living, she did require a 4 wheel walker for mobilization. Co-morbidities, not unusual for a lady of her years, did tend to be of the chronic nature. She had been receiving treatment from her GP for, atrial fibrillation(AF) controlled with warfarin and digoxin, diabetes mellitus Type 2 controlled with insulin and diet, irbesatran for hypertension, chronic leg ulcers for which she had had previous hospital admissions, and bilateral chronic lymphoedema, which may have developed following a hemicolectomy perform 5years previously, for bowel cancer. On presentation to the emergency department she was immediately transferred to the resuscitation area. A quick assessment of airway, breathing, and circulation, confirmed the initial assessment made by the GP. She was hypotensive, tachycardic, and febrile. She was exhibiting signs of the systemic inflammatory response syndrome (SIRS), presenting with two of the symptoms that meet the diagnostic criteria. However, having a known source of infection, altered mental state, and a significant decrease in systolic blood pressure, she was promptly diagnosed with severe sepsis, secondary to an infected leg ulcer. Severe sepsis being the early, or compensatory stage of shock (Garretson, 2007). Mrs M experienced the initial stage, as the normal inflammatory response failed to contain the bacteria. In the cell walls of bacteria is a substance called endotoxin, which, when lysis occurs is released in to the circulation. More than 40 different mediators are released, mobilizing an aggressive activation of the immune system, initiating the sepsis cascade (Crowley, 1996). As the inflammatory process continues, homostatic mechanisms are activated in an attempt to restore cardiac output, and tissue perfusion to vital organs. These mechanisms involve neural, hormonal and chemical changes (Tortora, 2000). The release of various chemical mediators during sepsis have both vasodialatory, and vasocontrictory properties, maldistribution of volume occurs, and a relative hypovalaema causes a drop in cardiac output.(Bridges, 2005). Mrs M's BP 68/40. Baroreceptors in the aorta, and carotid arteries, sense this loss of pressure, and via the control centre in the medulla oblongata, initiates a powerful sympathetic nervous response (Tortora, 20000. Activation of this system causes a redistribution of blood flow to vital organs, such as, the heart and brain, simultaneously diverting blood away from the less vital organs, such as the skin, lung, and kidney, by constricting blood vessels. The vasocontriction helps maintain venous return by, increasing systemic vascular resistance(SVR). However, due the reduced blood flow to kidneys, urine formation decreases, and the diminished flow through the lungs, impairs gas exchange.(Tortora, 2000). The release of the catecholamines adrenaline, and nor-adrenaline, stimulate the adrenergic receptors in the heart, increasing heart rate, and contractility, cardiac output improves. As the heart beats faster, and more forcefully, oxygen requirements increase, coronary arteries dilate, supplying more oxygen to the myocardium (Tortora, 2000).Mrs M's HR 115bpm. Decreased blood supply to the kidneys, causes them to secret renin, activating the renin-angiotensin pathway. The production of Angiotensin II causing a direct vasocontriction of arteries. This pathway also stimulates the adrenal cortex to secret Aldosterone. Aldosterone, a hormone that increases sodium re absorption, and, indirectly water, from the kidneys. Overall, increasing SVR and blood volume, helping increase blood pressure (Tortora, 2000). In response to the rising serum sodium levels, and a decreased blood pressure, the posterior pituitary gland releases Anti diuretic Hormone(Vasopressin) bringing about more vasocontriction, and water conservation. Cardiac output increases (Tortora, 2000). The redistribution of blood flow to priority organs, decreases pulmonary blood flow. Some alveolar containing oxygen ceases to be in direct contact with blood, this results in a ventilation/perfusion mismatch, and the development of hypoxemia (Elliot, 2008). Mrs M's Sa02 84%. This combination of decreased oxygen, and carbon dioxide in the blood, affects the level of consciousness, with the patient becoming restless, agitated, confused, and lethargic (Elliot, 2008). Mrs M's GP noted changes in her mental state ,and energy levels. In addition to a full clinical assessment, continuous cardiac monitoring was instituted, and frequent systemic observation attended, simultaneously, oxygen therapy at 8 litres a minute was administered via a non-rebreathing face mask to normalise oxygen saturation level, as is recommended by Robson,(2008). Two wide bore intravenous cannula were inserted, and fluid resuscitation commenced using an intravenous infusion of Gelofusin 500 ml given over 30minutes to increase blood pressure. Gelofusin, a colloid, which due to the large molecular size, remains within the intra vascular space. The oncotic pressure causing water to be drawn from the tissues, increases circulating volume, the effects of which can persist for several hours (Sumnall, 2007). With Mrs M's cardiac history of atrial fibrillation, and hypertension, there was a risk of her developing cardiac failure, and pulmonary oedema as a delayed reaction (Sumnall, 2007). but the greater need at this time was to restore circulating volume, and improve tissue perfusion. Due to the leg pain Mrs M was experiencing, Morphine 15 mgs intravenously was administered, in 2.5mg increments. At this time blood samples for full biochemical, and haematological screening was sent to the laboratory. Swabs taken from the leg ulcer, a urine sample, and sputum specimen, were sent to microbiology for culture and sensitivity As a policy of this hospital, due to the rising incidents of nosocomial infections, swabs from the nares, and groin for methicillin-resistant Staphylococcus aureus, and a rectal swab for Vancomycin-resistant Entrococci, were also sent for culture. A chest x-ray revealed no fluid or atelectasis, and an electrocardiogram (ECG) displayed atrial fibrillation, but no other abnormalities. Some hours later Mrs M was reviewed by the general medical team. She was found to be pale, and drowsy, which was not unusual as in addition to the opiates, she had also been given neurofen tabs 400mgs, panadiene forte II tabs, and endone 5mg tab orally. Her general condition however, seem to have improved, with her vital signs now displaying, BP110/65, AF 115bpm, Sa02 94% on supplemental oxygen of 4 litres/min, T 38.4C although still elevated, she had been commenced on a broad spectrum antibiotic. Blood results did show a few abnormalities. In keeping with infection, an increased C-reactive protein of 17mg/L, the normal being 0-10mg/L, was not unusual. Protein C is activated when thrombin interacts with endothelial cells ( a clotting enzyme that activates thrombin ), and has anti inflammatory, anti thrombolytic, and profibrinolyic effects (Bridges, 2005). A Troponin I level, which is a cardiac biomarker indicating myonecrosis, did show a small rise of 0.35, the normal being 0 – 0.15 (Heart Foundation, 2006). No chest pain had been experienced, and no ECG changes had been identified. At 19.30 hours that evening Mrs M was transferred to the acute observation ward onto a monitored bed. An intravenous infusion of 0.9% normal saline at 100ml/hr was given for hydration. An indwelling urine catheter was inserted to monitor her urine output, and being a Type 2 diabetic, a sliding scale insulin chart was commenced, titrating insulin doses to pre meal blood glucose levels, which up until this point had only been marginally elevated, with the highest recorded level being 10.2mmol/L. In view of the small Troponin rise, indicating myocardial ischaemia, Aspirin 300mg tabs, and Clexane 60mg subcutaneous was administered, serial ECG's , and troponin I levels ordered, which according to the guidelines for the management of acute coronary syndrome constitutes best practice (Heart Foundation, 2006). Mrs M's leg ulcer was attended, and dressed with a meliplex dressing. 3 hours later, the nursing staff observed a dramatic deterioration in her condition. The cardiac monitor was displaying AF 55bpm, BP and Sa02 were unrecordable. Her her conscious state had deteriorated to the point that she had become unrousable, a blood glucose level of 12.6mmol/L not accounting for the change. This prompted the nurses to call the medical emergency team (MET). At this hospital a flow chart is distributed to all clinical areas, which gives direction when patients fall into a certain category, such as, HR< 60bpm, BP