Nutrition in Acute Pancreatitis

Nutrition in Acute Pancreatitis

A 55-year-old previously healthy lady was admitted with pancreatitis secondary to gallstones. Her admission modified Glasgow Score was 4, and CT scan showed approximately 70% necrosis of the pancreas encompassing the neck, body and tail with sparing of the head. She rapidly developed ARDS, AKI and vasoplegia, and subsequently developed abdominal compartment syndrome requiring decompressive laparotomy. Her later complications included intraabdominal collections requiring percutaneous drainage, upper GI bleeding, and staged closure of her laparostomy. She was initially commenced on enteral NG feeding but developed high NG aspirates despite pro-kinetics. Parenteral nutrition (PN) was commenced in combination with a ‘trophic’ enteral feed. Four weeks into her admission her triglyceride level was found to be elevated, necessitating lipid free PN and cessation of propofol. This led to a drop in her triglyceride level.

How should we manage the provision of nutrition in acute pancreatitis?

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Corticosteroids in Septic Shock

Corticosteroids in Septic Shock

A week after an elective colectomy, a 70yr old man developed septic shock and multiorgan failure secondary to anastomotic breakdown. He was managed according to surviving sepsis guidelines with source control, early antibiotics, fluids and noradrenaline. The patient remained hypotensive and refractory to noradrenaline therapy, and had vasopressin and low dose hydrocortisone infusion commenced.

What is the evidence for the use of corticosteroids in septic shock?Read More »

Nutrition in the Intensive Care Unit

Nutrition in the Intensive Care Unit

A middle aged man is admitted with abdominal pain and vomiting. He has a history of alcohol excess. A CT scan shows evidence of pancreatic necrosis. Supportive care is initiated and an NGT placed for supplementary enteral nutrition. After 3 days, he is referred to ICU as his oxygen requirements have increased and he is requiring non-invasive ventilation. It is noted that he has had very large gastric aspirates. Parenteral nutrition is commenced at this point.

What is the evidence for enteral versus parenteral feed as a source of nutrition in critically ill patients?Read More »

Heparin Induced Thrombocytopenia

Heparin Induced Thrombocytopenia

A 62 year old lady with a metallic aortic valve was admitted to the cardiac unit for urgent surgical repair of a severely regurgitant mitral valve. He was normally on warfarin for his metal valve. This was stopped and unfractionated heparin commenced on day 4 once his INR level had dropped below the therapeutic range. The patient’s platelet count was 147*10^9/L on admission. By day 4 it had dropped to 85*10^9/L. After heparin was started it dropped further to a nadir of 55*10^9/L on day 8.

Could this be due to heparin induced thrombocytopenia? What investigations are required and how should we treat it?
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Hepatorenal Syndrome

Hepatorenal Syndrome

A 54 year old man with a history of alcohol excess was admitted under the medical team with an upper gastro-intestinal bleed. He had a background of pulmonary fibrosis that limited his exercise tolerance to 30 yards. Antibiotics, terlipressin and fluid resuscitation, including blood, were given. An oesophago-gastro-duodenoscopy demonstrated severe portal gastropathy but no active bleeding or varices. An abdominal ultrasound demonstrated cirrhosis and some moderate ascites. On day two of the patient’s hospital admission he was admitted to the intensive care unit (ICU) with respiratory failure and non-invasive ventilation was started. Over the next few days his condition deteriorated and he required vasopressor support. By day 6 the patient was oliguric, and his creatinine had risen from 102 to 155 µmoles/l.

What is the cause for his acute kidney injury? Could it be hepatorenal syndrome? Read More »

Hypertriglyceridaemia Induced Acute Pancreatitis

Hypertriglyceridaemia Induced Acute Pancreatitis

A young man is admitted to the surgical unit with several months of worsening abdominal pain. It has become much more severe over the last 24 hours. A CT scan shows evidence of acute pancreatitis with no gallstones or biliary duct dilatation.. He is normally well with no history of alcohol excess. His triglyceride level is elevated at 83.7mmol/L and a diagnosis of hypertriglyceridaemia induced acute pancreatitis is made. 

What is hypertriglyceridaemia induced acute pancreatitis and how is it treated?

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Decompressive Laparotomy in Abdominal Compartment Syndrome

Decompressive Laparotomy in Abdominal Compartment Syndrome

A 55 yr old man developed severe necrotizing pancreatitis with multiorgan failure. One week into his illness he had developed multiple intra-abdominal collections and had high intra-abdominal pressures. Initial conservative management failed, percutaneous drainage of his collections failed to reduce the abdominal pressures, and he underwent decompressive laparotomy.

What is the evidence behind the current guidelines for the measurement of intra-abdominal hypertension and the use of decompressive laparotomy in the management of Abdominal Compartment Syndrome?Read More »

Botulism

Botulism

A young female IV drug abuser presented with dysarthria, diplopia and weakness with loss of her gag reflex. She had recently had an abscess wound on her arm debrided. She was intubated for airway protection, and underwent early tracheostomy. She was treated with intravenous antibiotics and botulism antitoxin after electromyography and nerve conduction studies were consistent with a diagnosis of botulism. She was weaned from the ventilator within 2 weeks and the Health Protection Agency later confirmed the presence of botulism neurotoxin A from wound swabs.

What are the clinical features of Botulism and how is it managed?Read More »

Loop Diuretics in Acute Kidney Injury

Loop Diuretics in Acute Kidney Injury

A 65 year old woman underwent an elective mitral valve repair (MVR) and four vessel coronary artery bypass graft (CABG) procedure. Pre-operatively she was diagnosed with chronic kidney disease (CKD) secondary to hypertensive nephropathy, and chronic airway disease secondary to smoking. Her baseline creatinine was 275. Surgery was uneventful but in the post-operatively period she developed pulmonary oedema and worsening acute kidney injury (AKI). On day 2 her creatinine reached 420 and oliguria occurred (urine output < 0.5 ml kg-1 hr-1). Non-invasive respiratory ventilation provided adequate support and maintained a normal blood PaCO2 and pH, although her base excess drifted to -7 mmol l-1.Dopamine was administered at 2–10 μg kg-1 min-1, titrated to MAP ≧ 75 mmHg; pericardial pacing continued to maintain sinus rhythm at 60 bpm; her CVP was 14 mmHg and stable. Furosemide was started and given by a continuous infusion of 10 mg hr-1 after an initial bolus of 100 mg to try and help with diuresis.

Is there any evidence to support the use of loop diuretics in acute kidney injury?

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Glycaemic Control on the ICU

Glycaemic Control on the ICU

A 76 year old man with no comorbidities was admitted to the intensive care unit following an oesophagectomy. During routine blood sugar monitoring, his blood glucose was found to be just over 10 for two consecutive readings so he was commenced on a variable rate insulin infusion. Six hours later, despite hourly monitoring, he had a blood sugar of 3.6. The insulin infusion was stopped and his blood sugar rose back to normal levels. He suffered no apparent ill effects from his hypoglycaemic episode.

What is the rationale behind current glycaemic control on the intensive care unit?Read More »