Category: 2013

Management of Variceal Bleeding

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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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Propofol Infusion Syndrome

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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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Post-operative Opioid-Induced Hyperalgesia

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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 »

Facilitation Of Donation After Circulatory Death

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A previously fit and well 45 year old man presented to the emergency department with a two-hour history of a sudden onset severe headache associated with weakness, vomiting and photophobia. He had a normal breathing pattern and oxygen saturations of 96% in air. He was hypertensive with a non-invasive blood pressure of 220/115mmHg and a pulse rate of 85 beats/minute in sinus rhythm. Neurological examination revealed a Glasgow Coma Scale (GCS) of 14/15 with a dense hemiparesis, with hemisensory neglect and dysarthria.

He deteriorated and dropped his GCS to 5/15. He was intubated and an urgent computed tomographic (CT) brain scan was performed that revealed a large right-sided intraparenchymal haemorrhage with 4mm of midline shift. Blood tests including full blood count, urea and electrolytes and clotting screen were normal.

He was discussed with the neurosurgeons who felt transfer to institute intracranial pressure monitoring or surgical intervention was not indicated. His blood pressure was managed with a labetalol infusion aiming for a target systolic blood pressure of ≤ 160mmHg. Seizure activity was managed with a 15mg/kg loading dose of phenytoin followed by a maintenance dose of 300mg once daily nasogastrically. Sodium levels were monitored closely and hypotonic fluids avoided.

By day 5 he was making spontaneous respiratory effort, and his pupils were equal and sluggishly reactive. His GCS remained 3/15. A repeat CT was performed on day 9 due to no improvement in his clinical condition and revealed extension of the intraparenchymal haemorrhage with 8mm midline shift, effacement of the ventricles and loss of sulcal definition. A discussion regarding end of life care was held with his family who raised the possibility of organ donation. In agreement with his family, end of life care was instituted and he became an organ donor after circulatory death was confirmed.

How can we facilitate Donation After Circulatory Death?Read More »

Diagnosing Ventilator Associated Pneumonia

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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?

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Mechanical Ventilation of Chronic Obstructive Airways Disease

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A 68-year-old went into respiratory arrest on the chest ward. He had been admitted 2 weeks previously for an exacerbation of chronic obstructive airways disease (COAD). He has had two previous episodes of reduced conscious level due to hypercapnoea, which resolved with non-invasive ventilation and oxygen titration.

He was immediately intubated on the ward and transferred to the intensive care unit for ventilation. Hypoxia was corrected to a PaO2 >8.0kPa with a moderate FiO2. However he remained very difficult to ventilate and maintained a persistently high PaCO2. The highest level was 21kPa. He was treated with B2 agonist nebulisers, anti-muscarinic nebulisers, systemic steroids, aminophylline infusions, magnesium infusions and a ketamine infusion. He also needed vasopressor support and for a period of time continuous renal replacement therapy. After a week when his ventilator pressures reduced he had an uneventful percutaneous tracheostomy. Sedation was then reduced and he was awake and spontaneously breathing but with a high level of support. He was recurrently troubled by episodes of bronchospasm and air trapping. The lowest settings for inspiratory pressure were 14 cmH2O. He deteriorated a number of times before care was withdrawn and he died 20 days later.

Can we predict which COAD patients will benefit from mechanical ventilation?

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Enteral vs Parenteral Feeding on ICU

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A 70-year-old man had been an inpatient on the intensive care unit for nearly 40 days after a complicated recovery following mitral valve replacement. He was being gradually weaned from the ventilator via tracheostomy but required no other invasive organ support. His intensive care unit stay had been complicated by recurrent respiratory sepsis treated with antibiotics and aggressive physiotherapy. Up until this point he had been fed by a nasogastric tube but began to exhibit signs suggestive of impaired absorption including large nasogastric aspirates and a requirement for higher levels of parenteral electrolyte administration.

Prokinetic treatment with metoclopramide 10mg TDS for 24 hours failed to improve the high aspirate levels which remained in excess of 300ml every four hours. Erythromycin 250mg BD was added with little improvement. Following discussion with gastroenterology colleagues an agreement to place a post-pyloric nasojejunal feeding tube was made; unfortunately this procedure was delayed by a further 48 hours as no endoscopist was free to attend. Parenteral feeding was initiated at this point in order to maintain calorific intake.

Compare enteral and parental nutrition.Read More »

Echocardiography on ICU

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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 »

Albumin Use in Critical Illness

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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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Management of Refractory Intracranial Hypertension

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A young man with no significant past medical history was admitted to the Emergency Department following an assault. His Glasgow Coma Score on arrival was 8 with a motor score of 4 and there was evidence of an external head injury. Pupils were symmetrically reactive. He was intubated to facilitate further management. Both primary and secondary surveys were unremarkable apart from multiple contusions to the face and scalp. Multi-slice CT showed no intrabdominal or intrathoracic injury but significant intracranial pathology with subarachnoid and intraventricular blood and multiple, principally frontal contusions. No associated neuraxial fracture was seen.

Urgent neurosurgical opinion was sought which confirmed no immediate target for surgical intervention. The patient was transferred to the intensive care unit where appropriate monitoring was established including the insertion of a fibreoptic subdural intracranial pressure bolt. Initial intracranial pressure was measured at 18 mmHg. Sedation with propofol and alfentanil infusions was titrated to a RASS score of -3, ventilation adjusted to a PaO2 > 13 kPa and PaCO2 4.5-5.0 kPa as per the Brain Trauma Foundation guidelines and an infusion of noradrenaline started to achieve a cerebral perfusion pressure of 60 mmHg. The patient was nursed 30° head-up and although active cooling was not undertaken, temperature maintained at less 35-37.5°C.

There was initial stability but approximately 24 hours after admission sustained rises in intracranial pressure (ICP) in excess of 25 mmHg were seen, necessitating boluses of sedation, the addition of atracurium by infusion, administration of hypertonic saline, cooling to 35°C and brief periods of hyperventilation to a PaCO2 4.0-4.5 kPa albeit without significant control. Urgent repeat CT brain was undertaken which showed evolution of the contusions with signifiant oedema and loss of both the lateral ventricles and basal cisterns.

On further consultation, neurosurgical colleagues again felt that no immediate surgical option was viable; in particular that attempts to insert and external ventricular drain were unlikely to be successful and that contusionectomy would produce significant disability. The patient was randomised into the RESCUEicp trial and thiopentone infusion started at a rate to produce isoelectrical activity on three lead electroencephalogram.

What are the management options for refractory intracranial hypertension?
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