A 52 year old female was admitted to the ICU with septic shock secondary to cholangitis. She had liver cirrhosis secondary to alcoholic liver disease, although she had been abstinent since an admission with acute alcoholic hepatitis 2 years previously. She had recently entered the assessment pathway for orthotopic liver transplantation.
She presented to the Emergency Department with a short history of fever and confusion and falls. She was pyrexial, tachycardic and hypotensive. Her inflammatory markers were elevated and her liver enzyme profile suggested cholestasis. There were no other localising features on examination or preliminary investigation.
She was commenced in the ED on broad-spectrum antibiotic therapy (piperacillin-tazobactam) and fluid resuscitation consisting of Hartmann’s solution and 4% human albumin solution. Her blood pressure remained labile throughout the early part of her admission. She fulfilled the criteria for septic shock with evidence of evolving multi-organ dysfunction.
The patient received early, aggressive multi-organ support. Tracheal intubation and pressure-controlled ventilation were instituted due to grade III/ IV encephalopathy and a high work of breathing in response to profound metabolic acidaemia. A thorough clinical assessment of intravascular volume status was conducted, suggesting that the patient was adequately filled. Vasopressor therapy was initiated using noradrenaline to achieve a target MAP of 65mmHg. CVVHDF was commenced to control the severe acidaemia and hyperlactataemia.
The patient was vasoplegic and remained profoundly hypotensive despite rapidly escalating doses of noradrenaline and the addition of hydrocortisone. Continued assessment of intravascular status confirmed adequate filling and cardiac output monitoring using a pulse-contour analysis system confirmed a low SVRI- high cardiac output state. Her noradrenaline requirements soon exceeded 0.4mcg/kg/min-1, at this point a vasopressin infusion was introduced at 0.03units/hr-1. This was associated with an improvement in haemodynamic indices; the target MAP was achieved and thereafter remained stable with a slow reduction in noradrenaline requirement. On day 2 the continuous vasopressin infusion was converted to terlipressin by bolus dose regime (2mg QDS).
An urgent ultrasound scan of her biliary system revealed an obstructed common bile duct which was treated by percutaneous biliary drainage. An Enterococcus was isolated from drain fluid and blood cultures within 48 hours and antibiotic therapy tailored accordingly. The patient was weaned from organ support and discharged to the hepatology unit 9 days after admission.
What is the rationale for the use of vasopressin in septic shock? Are vasopressin analogues as effective?Read More »
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.
What adjunctive therapies, if any, are effective in the treatment of bacterial meningitis?Read More »
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.
Describe the incidence, clinical features and management of fungal infections in non-neutropaenic, non-transplant critical care patients.Read More »
A 68-year-old previously fit woman was admitted with left lower abdominal pain and signs of cardiovascular shock. She had had a 2 day history of crampy left lower abdominal pain and altered bowel habit. Clinically she had a diagnosis of bowel perforation with generalised peritonitis. She was exhibiting signs of shock with a pronounced tachycardia and a reduced systolic blood pressure.
She was started on fluid resuscitation and intravenous antibiotics. After her cardiovascular system stabilised she was taken to the operating theatre where she had a laparotomy. A sigmoid perforation was found with four quadrant faecal contamination. A Hartmann’s procedure was performed. A laparostomy was decided upon at the first instance, and was covered with a VAC dressing.
She was transferred to the intensive care unit (ICU) still intubated and ventilated.
Her condition rapidly worsened on the ICU. She required vasopressor support intra-operatively and her requirements rapidly escalated. She seemed to stabilse over the next 36 hours. Her condition then worsened and she was taken back to theatre for a washout of her peritoneal cavity. A number of collections were found and further soiling of her abdomen was evident. Her condition remained the same for the next 12 hours but then started to show an improvement again. She continued to make a good response to treatment over the next 3-4 days. She had another washout at 4 days. She was extubated on day 5 and invasive monitoring and cardiovascular support was no longer needed.
What is the role of laparotomy in the management of faecal peritonitis?Read More »
A 64 year old lady who had been admitted with acute pancreatitis due to gallstones. She was initially admitted to the intensive care unit for cardiovascular management and management of her electrolyte imbalance. After a few days she was intubated for hypoxia.
She developed pancreatic necrosis and pseudocyst formation. These were drained by percutaneous drains whereby she showed some improvement with more stability in her cardiovascular system. She had two failed extubations and then had a tracheostomy placed. She was weaned from the ventilator but then remained on 40-45% of oxygen for a number of weeks. Serial scans showed a static nature to her pseudocysts. Her inflammatory markers remained static at a moderate level over this time. It was felt that she had a ventilator associated pneumonia and was started on antibtiotics. She then showed improvement a number of days later. She was further weaned from the ventilator and decannulated. She needed recannulation later and suffered another episode of ventilator associated pneumonia which was treated. Eventually a number of months later she was discharged to the ward and then home.
How can we diagnose ventilator associated pneumonia?
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.
What are the clinical features of pneumococcal sepsis?Read More »
A 22-year-old female recent migrant presented at 31 weeks gestation (gravida 2 para 0) to the obstetric unit. She was complaining of diminished fetal movements. She had been well up to that morning but was complaining of increasing abdominal discomfort, and was becoming distressed. Examination showed she was not in labour but her abdomen was tender. Cardiotocograph showed a fetal heart rate of 130 bpm and poor variability. Two hours post admission, she was re-examined by obstetricians. Abdominal ultrasound failed to identify a fetal heartbeat. A diagnosis was made of intrauterine death, and initially a placental abruption was suspected. Ultrasound showed no thrombus and an intact placenta and so this was excluded. She was diagnosed as having a late miscarriage and the pain was assumed to be due to ongoing miscarriage. She was transferred to labour ward and a morphine PCA commenced for analgesia.
She received a dose of IV antibiotics on arrival to labour ward. At this point it was noted her oxygen saturations were falling and she was becoming increasingly drowsy, and this was felt to be due to sensitivity to the PCA. She was reviewed by obstetric anaesthetists who performed an arterial blood gas, which showed a marked metabolic acidosis with serum lactate of 6.3, and a diagnosis of severe sepsis was made. There was concern that the retained fetal material was the focus, and she was taken to theatre for emergency caesarian section. She was then transferred to ITU. By this stage she had developed established disseminated intravascular coagulation and pulmonary oedema. She developed rapidly worsening multiorgan failure and shock refractory to large doses of noradrenaline and died that evening, 8 hours post admission. Cause of death was found to be group A streptococcal sepsis.
What is the significance of sepsis in obstetric patients?Read More »
A 19 year old man presented to the surgical team complaining of abdominal pain. He underwent a laparoscopic appendicectomy and a perforated appendix was removed. He returned to the surgical ward and three days later was ready for discharge. Unfortunately he then developed worsening abdominal pain, fevers and breathlessness. He underwent a CT scan and this demonstrated multiple collections of infected matter within his abdomen in addition to bi-basal atelectasis. He was admitted to the intensive care unit for haemodynamic monitoring, oxygen therapy and broad spectrum antibiotics. He underwent three intra-abdominal washouts of infected material over an eight day admission. During this time he had attempted enteral feeding via a nasogastric tube but had very high gastric aspirates, with no absorption, as a result of a prolonged ileus. He was started on parenteral nutrition on day eight of his ICU admission.
When should parenteral nutrition be initiated in those that are failing to meet caloric targets with enteral feeding alone?
A young IV drug user was admitted with septic shock secondary to staphylococcal sepsis with bilateral shadowing on CXR. He rapidly required intubation due to hypoxia, and institution of vasopressor support. He had a significant metabolic acidosis and consequently was commenced on haemofiltration. Transthoracic echocardiography revealed a large tricuspid vegetation. After 48 hours of haemofiltration, his acidosis haf normalised, and pressor requirements had reduced. He had a prolonged respiratory wean before being transferred to a cardiothoracic centre.
What is the role of haemofiltration (or other modes of renal replacement therapy) in severe sepsis and septic shock? Read More »
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?