A 50 year-old man with a history of alcoholism attended to the emergency department having been found at home comatose.
He had a reduced Glasgow coma score on admission and was vomiting blood. He was not protecting his airway and was tachypnoeic, tachycardic and had a reduced systolic blood pressure. His oxygen saturations were low and there were coarse crackles on his chest. Old notes showed that on previous endoscopy oesophageal and gastric varices were found. He was cachectic with hepatosplenomegaly but no signs of ascites.. He was rumoured to be abstinent from alcohol and had been previously well up to one day ago when he was last seen. There was some report that he had been behaving oddly over the last 5 days though.
Supplemental oxygen was provided and the decision to intubate was made. An initial attempt to insert a Sengstaken-blakemore tube was abandoned until the patient was intubated using a rapid sequence intubation technique. The gastric balloon was inflated and put under tension. Blood tests showed a reduced haemoglobin level but no clotting abnormality. Transfusion of packed red cells was made.
Medical therapy included beginning a course of prophylactic antibiotics. Terlipressin was started at 2mg intravenously four times daily. He was also started on high dose proton pump inhibitors, lactulose and thiamine supplements.
The gastric balloon was left inflated for 10 hours and as there was no haemodynamic sign of further bleeding was then deflated. Oesophagogastrocopy the next morning on the intensive care unit showed only grade 1 varices with no recent stigmata of bleeding and some mild gastric erosions.
He continued to be haemodynamically stable and sedation was weaned. He did not wake up as expected on sedation hold and his ammonia level was found to be raised. Over the course of the next 2 days he improved and was extubated successfully and discharged to the ward.
A 42 year old female with type 2 diabetes presented to hospital with fevers, malaise and headache. She had become unwell 7 days earlier with coryzal symptoms, feverishness, and cough with green sputum. On examination she was unwell and intermittently drowsy but gas exchange was adequate and she was haemodynamically stable with lactate 1.5 units. Temperature was 39.6oC and glucose was 15.8 units. Chest x-ray showed bibasal consolidation. CRP was 35 units and white cell count was 12.9. She received ceftriaxone 2 g, clarithromycin 500 mg, intravenous crystalloid 1000 mL and an insulin sliding scale.
One hour after admission the patient deteriorated with GCS 6 and non-purposeful shaking movements of the right arm and leg, which resolved with diazepam 5 mg intravenously. Her airway became partially obstructed despite nasopharyngeal and oral airways and she was urgently intubated. Aciclovir 900 mg was given and the patient was transferred to the ICU.
CT head showed no abnormality. A lumbar puncture revealed turbid yellow-tinged cerebrospinal fluid (CSF). Dexamethasone 10 mg was given. A phenytoin infusion was started. Sedation was maintained with propofol and fentanyl.
The CSF showed Gram positive cocci and a white cell count of 1274 units with neutrophils 1248 units. CSF glucose was 0.3 units and protein was 5.5 g. Ceftriaxone twice daily and dexamethasone four times daily were continued and acyclovir was discontinued. Blood cultures and CSF both grew Streptococcus pneumoniae. Viral PCR was negative. After 48 hours the patient was extubated and then discharged to the ward without any neurological deficit. She went home 5 days after admission. Ceftriaxone was given for a total of 14 days, facilitated by the outpatient parenteral antibiotic therapy team. She was advised not to drive for 6 months.
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A 42 year old woman was admitted to the intensive care unit with necrotising pancreatitis. She required sedation and mechanical, vasopressors to maintain adequate mean arterial pressure and extensive crystalloid resuscitation. Enteral nutrition was initially maintained via nasogastric feeding. She was treated with empirical broad-spectrum antibiotics (meropenem) and was prescribed antifungal prophylaxis (fluconazole) at the request of the hepatobiliary surgical team.
The patient experienced a prolonged systemic inflammatory response syndrome. She ultimately underwent a pancreatic necrosectomy and required recurrent radiologically-guided percutaneous drainage of intra-abdominal collections. For a large proportion of her ICU admission, enteral nutrition failed and the patient required total parenteral nutrition. Candida albicans was isolated from central venous catheter exits sites, drain exit sites, drain fluid, urine and sputum on several occasions, but there was never any evidence of invasive fungal disease.
The patient was eventually discharged from ICU and survived to discharge from hospital. She was left dependent on pancreatic enzyme replacement and subcutaneous insulin therapy.
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A 65-year-old woman was admitted with a two-day history of feeling non-specifically unwell, severe upper abdominal pain, anorexia and vomiting. On examination she was tachycardic, hypotensive with epigastric tenderness and guarding. Admission amylase was 1024 mmol/L. A diagnosis of acute pancreatitis was made and she was admitted for conservative management with IV fluids and analgaesia. Her initial Ranson score was 3 placing her at moderate risk of of death. Abdominal ultrasound scanning showed a swollen pancreas with a small amount of free fluid but no gallstones or obstruction to the biliary system. Over the next twelve hours she deteriorated on the ward, developing type 1 respiratory failure for which she was referred to intensive care.
On admission to ITU she was semi-electively intubated and ventilated. A low-dose infusion of noradrenaline required to achieve adequate mean arterial pressure. A CT scan showed inflammatory changes and free fluid around the pancreas with possible early pseudocyst formation but no necrotic areas. Two hours after admission she became pyrexial at 39.5°C with a modest increase in her noradrenaline requirements. Peripheral blood cultures were taken and empirical imipenem started following discussion with microbiology. Subsequent repeated microbiological cultures of blood, ascitic fluid, urine and sputum were negative. A nasojejunal tube was passed to allow enteral feeding.
Over the next 48 hours her sedation was weaned and her respiratory function improved. Vasculitis screens, viral serology, lipids, etc. were all negative or normal. Despite her clinical improvement she remained pyrexial with an elevated CRP and white cell count. Further microbiological sampling was unhelpful, serum procalcitonin middling and repeat CT scan showed maturation of her pseduocyst. Fine needle aspiration was performed and subsequently proved culture negative. Her imipenem was stopped after 7 days after gradual resolution of her noradrenaline requirements. Surgical tracheostomy was performed on day 11 to facilitate ventilatory weaning and she was discharged to the ward on day 21.
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An elderly man with a background of ischaemic heart disease, severe aortic stenosis and type 2 diabetes mellitus presented following recent travel from Hong Kong with shortness of breath and hypoxia. A chest X-ray confirmed left lower lobe consolidation (CRP 502, WCC 22) and he was commenced on broad spectrum antibiotics (Tazocin and Clarithromycin). Over the following 12 hours he deteriorated on the ward, with worsening hypoxia, hypotension and anuria.
He required emergency admission to intensive care for intubation and ventilation, and required inotropic support. He developed a severe metabolic acidosis and rising lactate, for which haemofiltration was commenced. Vasopressin was added, followed by dobutamine, and hydrocortisone started for inotrope resistant hypotension. He remained ventilated on 100% oxygen, with high pressure support. He had a positive pneumococcal antigen, and high dose benzylpenicillin was added to his antibiotic regime, along with Oseltamivir (Tamiflu). Despite 12 hours of intensive therapy his acidosis worsened and he failed to respond to increasing doses of inotropic support, dying 30 hours after presentation to hospital.
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A 60-year-old alcoholic was admitted with large-volume, frank haematemesis. On presentation he was hypotensive, tachycardic and obtunded with multiple stigmata of chronic liver disease including a moderate volume of ascites and palpable splenomegaly. Initial phlebotomy revealed a haemoglobin of 6.4 g/dL, INR of 4.5 and bilirubin of 54 μmol/L. Arterial blood gas analysis demonstrated a significant metabolic acidosis and lactate of 11 mmol/L. Large bore intravenous access was established and administration of crystalloid initiated, targeting a systolic blood pressure of 90 mmHg. Urgent cross-match of 10 units of packed red blood cells, clotting products and platelets was requested and the patient was transferred to theatre where upper gastrointestinal tract endoscopy was performed under general anaesthesia. This demonstrated three columns of varices involving the gastro-oesophageal junction. Attempts at banding and injection of sclerosant met with variable success. A Senstaken-Blakemore tube was inserted due to incomplete haemostasis and further attempts at endoscopic therapy abandoned.
The patient was transferred to intensive care. Intravenous cefotaxime and terlipressin were commenced. Further transfusion of clotting products continued as guided by thromboelastography with some slowing of transfusion but red cell requirements persisted at a rate of 1-2 units of blood per hour. At 12 hours, repeat endoscopy was performed – further attempts at sclerotherapy were unsuccessful and transjugular intrahepatic porto-systemic shunting was performed by the interventional radiology team. Upon return to intensive care, a significant reduction in bleeding was noted and both haemodynamic indices and coagulopathy improved over the following 12 hours. A repeat endoscopy demonstrated no evidence of active ongoing bleeding. At this point sedation was stopped; some encephalopathy was evident although this improved in the following 24 hours. Extubation occurred on day 3 after admission and he was discharged to the high-dependency unit at day 5 without significant ongoing acute issues.
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 40 year old woman presented with painful swelling of the right side of the neck. She had previously suffered a haematological malignancy and received a bone marrow transplant. A presumptive diagnosis of necrotising fasciitis was made and the neck, shoulder and chest underwent surgical debridement. Postoperatively, the patient remained ventilated in septic shock. Further debridement was required at 24 hours. Group A streptococcus was grown from the debrided tissue and IV immunoglobulins was commenced. The patient gradually weaned from support and was discharged from ICU several days later.
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