A 50 year old female presented with acute kidney injury and sepsis. She required fluid resuscitation, haemofiltration and cardiovascular support for 2 days, following which she was discharged to the renal ward for on-going haemodialysis. She underwent dialysis every 2-3 days for the next 3 weeks. Whilst on the ward she deteriorated acutely one evening, developing respiratory distress, followed by a respiratory arrest. She was intubated and ventilated transferred to the critical care unit.
A CTPA was negative for pulmonary embolus, but showed large bilateral pleural effusions. Tracheal suctioning was initially clear but later copious blood stained secretions were removed. A bedside cardiac echo performed by the consultant intensivist showed a globally sluggish left ventricle, which was overfilled, and the inferior vena cava measured 3cm also suggesting fluid overload. A trial of furosemide failed and she was aggressively haemofiltered to remove the excess fluid. Troponin was only mildly raised, and not thought to be suggestive of an acute cardiac event. She was extubated 24 hours later, but had two further episodes of flash pulmonary oedema requiring non-invasive ventilatory support whilst haemofiltration was re-commenced for fluid balance reasons. In total twelve litres of fluid were removed, with significant improvement in the patient’s condition. Repeat echocardiography prior to discharge showed an improving left ventricular function and IVC measurement of 2cm with greatly increased compliance.
What is the evidence that focussed echocardiography helps guide decision-making in intensive care?Read More »
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 middle aged man presented with urosepsis after several days antibiotic therapy in the community. He was in septic shock, with tachypnoea, tachycardia and hypotension. He had raised inflammatory markers and acute kidney injury. His initial lactate level was 14mmol/L with a significant metabolic acidosis (base deficit 21). He was commenced on iv antibiotics, noradrenaline and renal replacement therapy. Lactate levels cleared to less than 2mmol/L over the next 24hrs. He weaned off noradrenaline in 72 hours and CVVHDF over the next 5 days.
How is lactate produced and what is its significance in predicting the severity of critical illness?
An elderly man was admitted after a Hartman’s procedure with primary closure for a perforated sigmoid diverticulum with four quadrant peritonitis. Postoperatively, he remained ventilated and noradrenaline dependent. His intra-abdominal pressures gradually rose from 15 to 24mmHg. Urine output was poor, and he required peak pressures of 28cmH2O to achieve 6ml/kg tidal volumes. Vasopressor requirements gradually increased and a diagnosis of abdominal compartment syndrome was made. Medical management was attempted with fluid resuscitation, increased sedation, aspiration of nasogastric tube and neuromuscular blockade. However this did not improve the intra-abdominal pressures so the patient returned to theatre laparostomy and VAC dressing. On return from theatre, intra-abdominal pressures stabilised between 12 and 15mmHg. Noradrenaline requirements fell and urine output improved. The abdomen was closed on day 5 and he was discharged from ICU on day 10.
What non-surgical strategies can be used to reduce intra-abdominal pressure?
A young adult female with known diagnosis of poorly controlled type 1 diabetes mellitus was admitted with out-of-hospital cardiac arrest. She had only recently been discharged from hospital after an admission with diabetic ketoacidosis. On arrival she had a GCS 3 with minimal respiratory effort. She was in profound DKA. Her temperature was 34.7°C on admission to ICU and she had targeted temperature management aiming for 36°C which was achieved within 2 hours. Her pH had normalised to 7.35 within 8 hours. 48 hours later one pupil became fixed and dilated. CT brain was consistent with global hypoxic ischaemic injury. EEG and SSEP on day 3 revealed severe lack of normal cortical activity. After discussion with family, treatment was withdrawn on day 4.
How do we undertake neuroprognostication after cardiac arrest in the post-TTM era?
A previously healthy 25 year old female was admitted with low GCS and a fever. She had a 24 history of viral symptoms including sore throat and a headache. On admission she had a GCS of 3, temperature of 38.9°C and raised inflammatory markers. She was intubated but did not require vasopressor support. A CT brain showed diffuse cerebral swelling, effacement of the sulci, sylvian fissures, basal cisterns and 3rd/4th ventricles, and early cerebellar tonsillar herniation. Lumbar puncture was not performed due to CT appearances. She was commenced on intravenous (IV) ceftriaxone 2g twice daily, IV acyclovir 800mg three times daily, and IV dexamethasone 10mg four times daily. Unfortunately, her pupils remained fixed and dilated on sedation hold 36 hours later, and she was making no respiratory efforts. She subsequently became a DBD organ donor.
What is the evidence for dexamethasone in bacterial meningitis?
A 85 year old man presented with acute bowel obstruction. He had a history of hypertension and diverticulitis disease, but was active for his age. He was not known to have coronary or any other vascular pathology. At laparotomy, a large diverticulitis abscess was identified. When this was manipulated, he developed an SVT with a ventricular rate of 210 bpm which progressed to VT. He received 1 mg adrenaline and 2 minutes CPR in total, with no electrical shocks. At this point perfusion and pressure returned. Surgery was expedited and simplified. He remained intubated and ventilated on ITU post-operatively. ECG demonstrated global t-wave inversion. He required noradrenaline and adrenaline to maintain blood pressure. During the initial 48 hours, his haemoglobin (Hb) fell from 11.9 g/dl to 8.1 g/dl, raising the suggestion of packed red cell (PRC) transfusion.
What is the most appropriate threshold to transfuse packed red cells in critically ill patients?Read More »
A 34 year old IV drug abuser was admitted with respiratory failure, bilateral patchy changes on chest X-ray, raised inflammatory markers and septic shock. She was intubated and commenced on antibiotics and noradrenaline. An in-house Focussed Intensive Care Echo was performed to guide fluid resuscitation. This was suggestive of hypovolaemia, but a large mobile mass was also observed in the left ventricular chamber. A departmental echo the next day confirmed the presence of a large vegetation on the anterior mitral valve leaflet with severe mitral regurgitation. She underwent a further period of stabilisation and underwent a mitral valve replacement.
What is the evidence for the development of in-house echocardiography skills within the critical care setting?Read More »
A 40 year old man underwent a minor elective day case lower limb soft tissue operation. 72 hrs later he began to feel unwell and developed fevers and rigors. He was seen first thing in the morning with increasing pain and inflammation extending up from the foot to the knee. Intravenous antibiotics were started on admission. He was in theatre having a debridement by late morning, by which time the inflammation had spread to the inner thigh. He was in profound septic shock with disseminated intravascular coagulopathy. During the debridement, it was noted that the inflammation had spread to his pelvis. He had a laparotomy and it was determined that the resection he would require was unsurvivable. Treatment was withdrawn and he died on the operating table.
How is necrotising fasciitis diagnosed and how is it managed?
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 »