A 40 year old was admitted to hospital with his first presentation of alcoholic liver disease with symptoms of jaundice (bilirubin 248), poor mobility, hallucinations and passing of black stool. On admission to hospital, he was lethargic with features of Grade II encephalopathy, was coagulopathic (INR 3.1), had deranged electrolytes (sodium 114, potassium 2.9), but a normal creatinine (54) and a raised white cell count (15.9). He was haemodynamically stable and had a haemoglobin of 119g/L with no signs of active bleeding. His abdomen was distended (ascites), he was visibly jaundiced and had spider naevi on his chest. An abdominal ultrasound was performed that showed liver cirrhosis, borderline splenomegaly, small volume ascites and normal kidneys. A full liver screen revealed no infective cause and his AST:ALT ratio suggested alcoholic liver disease. His prognostic indicator scores were all suggestive of severe alcoholic liver hepatitis (Maddrey score: 131; Childs: C; Lille Score: 1; GAHS: 10; MELD: 29). His serum ammonia level was 170. He was commenced on terlipressin, prednisolone and pentoxyphylline and thiamine. Despite this, his encephalopathy progressed to grade 4 and he required intubation and ventilation for airway protection and a presumed aspiration pneumonia. His liver function and coagulopathy continued to worsen, and he developed an acute kidney injury necessitating commencement of renal replacement therapy. He required noradrenaline to support his blood pressure. Ascitic tap ruled out spontaneous bacterial peritonitis. He was discussed with regional liver centres, but was not felt to be a transplant candidate. His liver and renal function continued to deteriorate and eventually treatment was withdrawn nearly 3 weeks into his admission.
Describe the scoring systems for assessing the severity of acute hepatic dysfunction.
A 40 year old female presented with a severe sudden onset headache, and deteriorated in the emergency department with worsening agitation and confusion requiring intubation and ventilation for her own safety. A CT scan diagnosed a Fisher Grade 4 subarachnoid haemorrhage and obstructive hydrocephalus. Clinical presentation was scored as Hunt and Hess grade 4 or World Federation of Neurosurgeons grade 4. The patient was transferred to the local tertiary Neurocritical care unit where an extra-ventricular drain was inserted overnight. The following day the patient underwent coiling of her right middle cerebral artery aneurysm in the radiology suite. A Magnesium infusion and Nimodipine therapy were commenced to reduce the risk of vasospasm. On initial sedation hold she woke up agitated so she had an early tracheostomy placed to allow controlled wake up. She had a straightforward respiratory wean from the ventilator over the next few days. Neurological recovery was good (Glasgow coma score improved to 14/15) and the patient was discharged to the ward for on-going neuro rehabilitation and repatriation to the base hospital.
What are the risks of clipping vs coiling subarachnoid haemorrhages?Read More »
An elderly man was admitted with an acute abdomen and free air visible under the diaphragm on CXR. He was fluid resuscitated before undergoing emergency laparotomy, where a perforated duodenal ulcer was oversewn. He was admitted to ICU postoperatively, extubated the next morning and deemed fit for discharge to the surgical ward later that day. Due to a lack of surgical beds, he was eventually discharged from ICU at 22:30. Eight hours post discharge, he was urgently re-referred to ICU after being found moribund on the ward. Before he could be seen and assessed he suffered an unrecoverable asystolic arrest. Review of his observation charts showed that there had been a clear deterioration in recorded observations, including hypotension for the two preceeding hours. However, the Early Warning Score had been calculated incorrectly, and no escalation had occurred.
What evidence is there that rapid response systems are effective in preventing patient deterioration and improving outcomes?
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?
A 30 year old woman with a background of substance abuse and deliberate self harm was found collapsed and semi-conscious following an overdose of co-codamol and was presenting late. It was possible that she had taken around 100g paracetamol. Her GCS was 11, and she had grade II/III hepatic encephalopathy. Her bilirubin was 60 and she had significant transaminitis with a lactic acidosis. . She was commenced on N-acetylcysteine despite undetectable paracetamol levels. Liver US was normal. Early repeat bloods showed worsening jaundice, transaminitis and rising INR. She was transferred to the regional liver unit initially for monitoring, but was subsequently admitted to the liver HDU. She did not require a liver transplant and recovered with conservative management.
What is the optimum management of hepatic encephalopathy in acute liver failure?Read More »