Albumin for Resuscitation in Critical Illness

 

A 50-year-old man was brought to the emergency department. He had sustained a burn affecting 55% of his total body surface area and a significant inhalational injury.  In the emergency department he was intubated and ventilated, central venous, arterial and urinary catheters were placed and resuscitation begun using the Parkland formula.

He was transferred to burns intensive care.  Fluid resuscitation was continued using Hartmann’s solution.  A bronchoscopy was performed; 1.26% sodium bicarbonate was used for lavage.  He became increasingly tachycardic and hypotensive.  He was oliguric.  His haematocrit was 0.45.  Fluid status was difficult to assess clinically; he felt warm to touch.  An oesophageal Doppler probe was sited which demonstrated low stroke volume and corrected flow time.  His Doppler parameters improved with each 250ml bolus of Hartmann’s solution but the effect was short lived.  Noradrenaline and then adrenaline infusions were used in an attempt to maintain blood pressure.  After a significant volume of crystalloid had been given, approximately 12 hours after the time of injury, 4.5% human albumin solution was requested.  This seemed to have a more prolonged effect than Hartmann’s solution.  Over the next 12 hours the patient’s haemodynamic status stabilised and he was able to undergo initial surgical management of his burn 36 hours after presentation.

What is the evidence for the use of human albumin solution for fluid resuscitation in critically ill patients.Read More »

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Management of Variceal Bleeding

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.

Describe the management of variceal bleeding.

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Vasopressin Versus Vasopressin Analogues in Septic Shock

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 »

Propofol Infusion Syndrome

A 28-year-old man was involved in a high-speed road traffic accident suffering severe head injury (diffuse axonal injury) with bilateral haemopneumothoraces and pulmonary contusions. He was transferred intubated and ventilated to the neurointensive care unit from a district general hospital for intra-cranial pressure (ICP) monitoring.

He was initially managed with bilateral chest drains and conservative neuroprotective measures for difficult to control ICP. He was heavily sedated on propofol (300mg/hr), midazolam (30mg/hr) and fentanyl (300mcg/hr).

Over the next few days his temperature increased and he became increasingly hypoxic. He subsequently developed ECG changes and a echocardiogram showed right heart failure. A diagnosis of pulmonary embolism, which was confirmed on CTPA a few days later which showed evidence of a small PE. He was not anticoagulated due to neurosurgical concern regarding his head injury.

Over the next few days he developed renal failure requiring renal replacement therapy and acute liver failure with hypoglycaemia and lactic acidosis. He developed severe cardiovascular failure requiring multiple inotropes and pulmonary artery catheter guided therapy. Lipids were found to be elevated, with creatine kinase >50,000 and myoglobin found in the urine. Propofol infusion syndrome was diagnosed. Sedation was stopped and he started to make a recovery.

What are the clinical features of propofol infusion syndrome?

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Adjunctive Therapies in Bacterial Meningitis

 

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 »

Thrombolysis and Intermediate-Risk Pulmonary Embolism

 

A 40 year old woman was admitted to the emergency department (ED) after a syncopal episode. On admission she was in acute respiratory distress and described a two day history of sudden onset breathlessness. She had no previous medical history. Her only regular medication was the oral contraceptive pill. She had had a recent flu-like illness and been less active than usual. On arrival she had a respiratory rate of 30 breaths/minute with accessory muscle use. An ABG on 15L/min oxygen via non-rebreathe mask showed type I respiratory failure (PO2 8.4kPa). She was tachycardic (120bpm) and blood pressure was 98/50. Chest x-ray and bloods were unremarkable although her ECG revealed a sinus tachycardia with right axis deviation, Q waves and inverted T waves in lead III.

The patient had a bedside echocardiogram that revealed a severely dilated right ventricle with poor tricuspid annulus planar systolic excursion (TAPSE). A presumed diagnosis of a pulmonary embolism (PE) was made. Thrombolytic therapy was considered but rejected at this point, in view of the haemodynamic stability. The patient was commenced on enoxaparin at a dose of 1.5mg/kg.

CT pulmonary angiography confirmed the presence of bilateral pulmonary emboli. On return from CT the patient was sat up briefly at which time she became cyanotic and had a brief self-terminating seizure. During this time her blood pressure was not recordable, and significant hypotension secondary to obstructive shock was assumed to be the cause. At this point it was decided to proceed with thrombolysis. The patient was transferred to the Intensive Care Unit, made a rapid recovery without the need for vasopressors or intubation and ventilation, and was discharged from hospital a few days later.

What is the evidence for intravenous thrombolysis for intermediate-risk pulmonary embolism? Read More »

Massive Propranolol Overdose

A 35 year old male presented with massive (over 1500mg) propranolol overdose on a background of depression and anxiety. He called for help and was found alert and cardiovascularly stable by paramedics at 50 minutes post ingestion. By 80 minutes his conscious level had fallen to a Glasgow Coma Score of 11 and he had become hypotensive. He started fitting en route to hospital and lost cardiac output as he arrived at hospital. The initial cardiac arrest rhythm was broad complex slow pulseless electrical activity. After a prolonged resuscitation attempt he regained spontaneous cardiac output but never achieved cardiovascular stability and sadly died later that evening.

He was resuscitated according to standard resuscitation algorithms. In addition, several specific therapies were given in line with Toxbase recommendations1: Glucagon was administered as a 10mg slow bolus followed by a 100-150 mcg/kg/hr infusion. Insulin (actrapid) was given as a 60 unit bolus followed by a 1-2 unit/kg/hr infusion along with a glucose bolus of 0.5 g/kg followed by an infusion of 0.5 g/kg/hr. Intralipid was delivered as a bolus (100 ml 20%) followed by an infusion. Atropine 3mg was given and the adrenaline boluses were changed to an infusion at 10 mg/hr.

Cardiac arrest remained refractory until a 100 ml bolus of 8.4% Sodium Bicarbonate was administered prompting almost instantaneous restoration of circulation.

The circulation remained unstable with a broad complex bradycardia resistant to transcutaneous pacing. High dose adrenaline infusion, high dose euglycaemic insulin therapy and glucagon infusion were continued. Transvenous pacing was also ineffective and the patient sadly deteriorated into a refractory cardiac arrest from which he did not recover.

The patient regained his cardiac output when the sodium bicarbonate bolus was given. The temporal association between these two events was profound and led me to question why this therapy sits so far down the toxbase treatment algorithm.1

This case summary aims to answer: 

  1. What works in Propranolol overdose? 
  2. What doesn’t really work? 
  3. Which order should I give things?

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Post-operative Opioid-Induced Hyperalgesia

 

An elderly female was admitted to the intensive care unit (ICU)following a planned hemi-hepatectomy to remove metastatic lesions from a previously resected primary colorectal cancer. The patient had declined neuraxial anaesthesia. The surgery proceeded uneventfully via a rooftop incision under general anaesthesia, which was maintained with remifentanil, sevofluorane and paralysis with atracurium.

30 minutes before the termination of the three hour operation, a bolus of 10mg of morphine was given intravenously and a patient-controlled analgesia (PCA) morphine pump was prepared. At emergence from anaesthesia, paralysis was reversed, and the patient was successfully extubated. In the ICU the patient was instructed in the use of the PCA. She was initially comfortable, but within 30 minutes she complained of worsening abdominal pain around the upper abdominal incision and became tachycardic.

To address this patient’s worsening post-operative abdominal pain 10mg of morphine was given intravenously. Simultaneously she was reassessed and the potential cause of the pain was sought. The abdomen remained soft and mildly tender. Drains were dry, and parameters including blood pressure, respiratory rate, haemoglobin, and arterial blood gases were satisfactory.

The morphine was ineffective. She was given 1g of intravenous paracetamol, a further bolus of 10mg of morphine and two sequential 500mL aliquots of crystalloid. Surgical review was requested. After another 20 minutes the pain had not diminished so she received a bolus of fentanyl and a trial dose of 100mg of intravenous tramadol. Unfortunately these measures did not reduce the pain at all. Although vital signs were unchanged, the patient was increasingly distressed.

There was no apparent clinical deterioration to account for the increased pain. Yet, control of her symptoms had clearly been lost and routine analgesia was ineffective. Urgent senior review was requested. Suspecting that she had become refractory to opioid analgesia, and concerned about the severity of the pain and its potential complications, the consultant stopped the patient’s PCA, increased the inspired oxygen fraction to 0.80 through a non-rebreathe mask, and gave 50mg of ketamine intravenously.

These interventions significantly improved symptoms over the next ten minutes. The patient remained conscious though slightly drowsy and her tachycardia settled. Simple analgesics and a low dose infusion of 2-5 mcg/kg/min (approximately 10-25 mg/h) of ketamine were prescribed. These effectively controlled her pain. After the patient had remained comfortable and clinically stable for several hours, the PCA was gradually re-introduced and the ketamine was discontinued. She was discharged to the ward the following day.

What is opioid-induced hyperalgesia?Read More »

Dexmedetomidine Sedation and Delirium

A 35-year-old man was admitted through the Emergency Department with a three-day history of sore throat, drooling of saliva and fever. In the twenty-four hours leading up to his admission he had reported increasing difficulty breathing and hoarseness. His past medical history included obesity and non-insulin dependent diabetes mellitus.

On initial assessment he was found to be stridulous, drooling, tachypnoeic, tachycardic and febrile. Supplemental oxygen was applied and intravenous access obtained, with blood cultures being sent prior to administration of broad-spectrum antibiotics (Ceftriaxone, Benzylpenicillin and Metronidazole). Despite nebulised Adrenaline, intravenous fluid and intravenous dexamethasone, he continued to deteriorate and was transferred to the anaesthetic room for definitive airway management. Findings at intubation were consistent with acute epiglottitis. Swabs were taken and oral fibreoptic intubation was successfully performed.

Following admission to the ICU, he was mechanically ventilated and sedated with infusions of Propofol and Remifentanil. Antibiotic therapy was continued and he was commenced on regular dexamethasone to reduce epiglottic oedema. He required a low- dose noradrenaline infusion to maintain blood pressure, and was commenced on an insulin sliding scale. Two days after admission his airway was reassessed with direct laryngoscopy, and was found to be significantly less oedematous.

At this stage a sedation hold was performed, with the patient opening eyes spontaneously and seeming to obey commands. He was extubated to humidified facemask oxygen but shortly afterwards became agitated, combative and delirious (CAM-ICU positive). The patient was re-intubated within a two-hour period and Propofol and Remifentanil sedation was recommenced. Over the following two days, he remained inappropriate on daily sedation holds, and by this stage was receiving bolus doses of Haloperidol for episodes of acute agitation. CT imaging of his brain revealed no abnormality, and lumbar puncture was negative for central nervous system infection. Intravenous dexamethasone had been weaned, in view of the improvement in epiglotittis seen at laryngoscopy.

By day six of his admission he remained neurologically inappropriate on sedation hold, and was changed to an intravenous infusion of Dexmedetomidine at 0.7 mcg/kg/hr. Remifentanil was weaned off at this time, and Propofol infusion was reduced to baseline levels. This continued for a further twenty-four hours, by which time he was neurologically appropriate on sedation hold, obeying commands, and was extubated uneventfully.

On direct questioning, the patient did not recall his first extubation episode on Intensive Care. He did recall a combination of vivid visual and auditory hallucations, including the presence of insects in his bed, hearing persecutory voices and a feeling of helplessness and fear. He made a full recovery, and these symptoms had fully resolved by the time he was discharged from hospital.

What is the role of dexmedetomidine in the prevention and management of ICU delirium?

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Albumin Use in Critical Illness

A 70-year-old woman was admitted to the surgical ward with abdominal pain. CT scans showed some dilated loops of small bowel. She remained on the surgical ward for 5 days with minimal resolution of her symptoms. She was taken to theatre for exploratory laparotomy where she was diagnosed with faecal peritonitis from a perforated diverticulum. She had a washout and a Hartmanns procedure was performed.
She became unstable during her laparotomy requiring vasopressors and was taken to the intensive care unit postoperatively.  She was left with a laparostomy with a VAC dressing applied. She was treated with lung protective ventilation and remained cardiovascularly unstable. Two days later she was taken back to theatre for a further washout and closure of her abdomen. She developed an ileus and was then started on total parenteral nutrition. An oesophageal doppler monitor was placed to help guide her fluid status. She was extubated on day 4 post op but her filling status remained a problem to gauge. Her fluid balance became very positive and she became very oedematous. Her albumin level dropped significantly. It was then decided to give her daily intravenous albumin.
What evidence is there for the use of albumin in critically ill patients?

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