Category: Year

The year that the Case Summary was written (if known).

Management of Inhalational Injury

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A 30-year-old man with no significant past medical history was admitted to ED from a house fire started by a piece of faulty electrical equipment. There were superficial skin burns only but some evidence of a possible inhalation injury with singed nasal hairs and a hoarse voice. Coughing resulted in expectoration of carbonaceous sputum with some haemoptysis. Arterial blood gas analysis revealed a PaO2 of 10.4 kPa on 40% oxygen a carboxyhaemoglobin level of 18%.

Semi-elective endotracheal intubation was performed using an uncut orotracheal tube. Ventilatory parameters were adjusted to give a tidal volume of 6-8 ml/kg and plateau pressure of less than 30 cmH20. Recruitment manouveres were performed to give an optimum compliance in the region of 40-50 ml/cmH20 with a positive end-expiratory pressure of 8 H20. The inspired fraction of oxygen was kept high (i.e. greater than 60%) until there was a fall of the carboxyhaemoglobin level to less than 5% at which point downwards titration was performed as guided by a target SpO2 of 94%.

Fibreoptic bronchoscopy was performed approximately six hours after admission to intensive care which demonstrated carbonaceous colonisation of the lower respiratory tract and areas of erythematous and denuded epithelium. Within 12 hours of intubation significant oedema of the face and upper airway had developed. A restrictive fluid regimen was instituted and there was gradual resolution of this swelling over the next 3 days. At this time, gas exchange was satisfactory and the patient was successfully extubated before being discharged to the high-dependency unit.

How is inhalational injury managed on the ICU?Read More »

Pneumococcal Sepsis

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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.

What are the clinical features of pneumococcal sepsis?Read More »

Advance Directives

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An elderly man presented to hospital with an acute abdomen. He was fit and well, with a background of well-controlled hypertension and chronic back pain. He had previously had admissions with a recurrent gastric volvulus, each time it had resolved spontaneously.

A CT scan was performed and revealed a gastric volvulus which was decompressed endoscopically. He was transferred to the high dependency ward post-procedure for observation as it was deemed high risk for recurrence and therefore likely that he would need surgery to correct it. Overnight he required increasing amounts of fluid and analgesia and suddenly deteriorated with a tachycardia, rising lactate and peritonitic abdomen. He was taken for an emergency laparotomy and had a gastrectomy. A feeding jejunostomy was inserted during the procedure.

The post-operative course involved a period of septic shock and multi-organ failure. He remained intubated, on a noradrenaline infusion and was receiving CVVH for renal failure. On the third post-operative day, despite a 24 hour sedation hold, he was showing no sign of any neurological recovery and was not eye-opening or obeying commands. It was at this point that his wife presented the team with an advance directive.

The advance directive was presented at a point in the care whereby the patient was already receiving high levels of support for his cardiovascular system (noradrenaline 0.3mcg/kg/min), respiratory system, renal system (CVVH) and gastrointestinal system (jejunostomy feed). It was discussed and a plan was made to, for the current time, continue management, but it was explained that the outlook was bleak.

His renal function worsened over the next few days (urea 27, creatinine 400) and despite a long sedation hold, he was still unable to obey commands. However,care was continued as both the cardiovascular and respiratory support was decreasing, with the noradrenaline having been weaned by day 6. He was extubated by day, but remained mildly confused and agitated. The following day, he became more tachycardic, tachypneoic and hypotensive. He deteriorated significantly to the extent where he became peri-arrest and was re-intubated. A CT confirmed an intra-abdominal/mediastinal catastrophe.

He once again developed severe septic shock with multi-organ dysfunction. His antiobiotics were restarted (meropenum) and an anti-fungal (fluconazole) introduced. NJ feed was commenced. He improved to the point of extubation on day 11, but again deteriorated. At this point, a decision involving his wife was made to palliate him. He died later that day

What are the implications of advance directives on the ICU?Read More »

Use of Bicarbonate in Lactic Acidosis

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Five days post emergency colorectal surgery, an elderly woman, following a brief period of chest pain a few hours earlier, developed progressive hypotension and tachycardia on the ward. She had a background of hypertension, type 2 diabetes and a chronic left foot ulcer. On examination she was found to be clammy, mottled and peripherally vasoconstricted with a GCS of 15/15. Her abdomen was soft and non-tender. Her initial ECG had showed no ischaemic changes and subsequent ECGs showed only a sinus tachycardia.

Initial blood gas analysis showed a metabolic acidosis (pH 7.21 Lactate 2.8mmol/l, HCO3 11.1mmol/l with a pCO2 of 2.7kPa).  A starting differential diagnosis of a cardiac event, a pulmonary embolism, critical ischaemia or sepsis related to a hip or foot ulcer were made. Urgent orthopaedic and vascular review were obtained, and it was deemed that neither the hip, ulcer or vascular insufficiency were a likely source for the deterioration. Initially it was planned to transfer her for a CTPA, however she became progressively unstable, was no longer fluid responsive, and was intubated on the ward and transferred to the intensive care unit (ICU) for stabilisation.

On arrival on ICU she continued to deteriorate, and in addition to fluid resuscitation required a high dose noradrenaline infusion to maintain her blood pressure. Broad spectrum antibiotics were started, a bedside echocardiogram and blood tests performed and hydrocortisone started. Her metabolic acidosis continued to deteriorate, subsequent arterial blood gas showed a pH 6.91, Lactate of 13.7mmol/l, HCO3 7.7mmol/l, base excess -25mmol/l with a pCO2 of 5.4kPa. It was decided to correct this acidosis with a bicarbonate infusion and initially 200ml of 8.4% was given over an hour, based on correcting half the calculated bicarbonate deficit (bicarbonate deficit (mmol) = base deficit 0.3xbodyweight(kg)1).  The blood gas following this infusion showed improvement in the metabolic acidosis despite the increasing Lactate (pH 7.07, Lac 14.0mmol/l, HCO3 10mmol/l, BE -18.6mmol/l with a pCO2 of 4.85kPa). She continued to deteriorate and the results from her blood tests, troponin and bedside echo suggested a primary myocardial infarction to cause this decline. She was too unstable for primary coronary intervention and her condition continued to deteriorate. She died 6 hours post admission.

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High Dose Insulin Infusion for Calcium Channel Blocker Overdose

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A 24-year-old was admitted following an intentional overdose of 10mg amlodipine tablets following an argument with his family. Approximately 10 tablets were ingested. On self-presentation two hours after the event, he was clinically stable with no haemodynamic compromise. There was no airway or respiratory compromise and a 12 lead electrocardiogram demonstrated sinus rhythm at 98 beats per minute. Both an arterial blood gas and electrolyte analysis were normal. Ionised calcium was 1.14 mol/L.

Over the following two hours he developed hypotension down to a nadir of 58/32 mmHg without change in heart rate or rhythm or the development of metabolic abnormalities. This was initially treated with intravenous fluids without significant response. A bolus of calcium chloride was administered without success; at this time he was referred to the intensive care team for assessment. Careful clinical examination revealed no other abnormality except hypotension. Neurological function remained intact and there appeared to be a vasodilated state with warm peripheries and relative tachycardia at 110 beats per minute in sinus rhythm.

The patient was transferred to the intensive care unit where an infusion of noradrenaline was commenced, rapidly escalating to a rate of 0.92 mcg/kg/min with little improvement in mean arterial pressure beyond 30-40 mmHg and relative oliguria. After consultation with the National Poisons Service, a high dose infusion of actrapid was commenced at rate of 0.5 units/kg/hour, with subsequent improvement of his haemodynamic parameters and a reduction in his noradrenaline requirement. Over the following 4 hours, both this infusion and the noradrenaline infusion were subsequently weaned off. The patient was discharged to the ward after eight hours and after assessment by the psychiatric team, from hospital the following day.

What are the clinical features of calcium channel blocker overdose and what is the role of high dose insulin infusion?Read More »

Massive Transfusion in Upper Gastrointestinal Haemorrhage

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A 55 year old male presented with acute upper abdominal pain and haematemesis. He had admitted drinking alcohol to excess. Following admission, he had a further significant episode of haematemesis associated with haemorrhagic shock. An emergency oesophagogastrectomy (OGD) was arranged in theatre. His pre-procedure haemoglobin was 60g/L.  OGD revealed large amounts of fresh blood in the stomach, which prevented identification of the bleeding point. The patient had a number of oesophageal varices, attempts were made to band these but this did not stop the bleeding. A partial gastrectomy was undertaken. The patient received a total of 18 units of red blood cells, 14 units of flesh frozen plasma and 2 units of platelets and cryoprecipitate before being taken to Intensive Care intubated and ventilated.

On the Intensive Care Unit he was warmed and repeat blood tests were sent to ensure correction of his coagulopathy. Haemoglobin was recorded as 9.4g/dL and the APTTr was normal. The following day when he was normothermic and cardiovascularly stable he was woken and extubated. He was discharged to the ward the following day.

When should we transfuse in upper gastro-intestinal haemorrhage? Are there any adjunctive therapies that can help?Read More »

Attempted Suicide and Treatment Withdrawal

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A elderly man  was found unconscious at home having taken an overdose of prescription medication. This event may have been precipitated by a recent bereavement and worsening of his preexisting depression for which he had recently been reviewed by psychiatric services and commenced on an SNRI. He left a note at the scene of the suicide attempt, clearly stating that he intended to take his own life and did not wish to be resuscitated in the event of being found alive. He was discovered in his home by a relative who had been growing increasingly concerned as to his welfare, having not spoken to him for several days. On arrival in ED his Glasgow coma score (GCS) was 3/15. He was known to be taking venlafaxine for depression and amitriptyline for chronic back pain, and empty packets of each drug were found at his home.

He was intubated and transferred to the intensive care unit. Supportive care was provided including vasopressors (noradrenaline) for hypotension, electrolyte correction and ventilatory support. Plain chest radiograph showed a probable aspiration pneumonitis affecting the right upper and middle lobe. He was hypoxic with a high Fi 02 requirement and needed high levels of PEEP to maintain adequate oxygenation. His conscious level fluctuated over several days and he became increasingly agitated and exhibited signs of distress. At this stage it was not clear if he was orientated in time, place or person. He underwent percutaneous tracheostomy to facilitate weaning and reduce sedation requirements.

We were then able to wean him from sedation by day 11 of his admission. The patient’s ventilatory requirements were still high requiring mean airway pressures of 30 cmH2O, PEEP of 10 cmH2O, and an inspired oxygen concentration of 60%. At this stage he indicated to the ITU team that he did not wish treatment to be continued. We found him to be fully orientated in terms of time and place and he was aware of the preceding events and his intentional overdose. It was clearly explained to him that if treatment were discontinued he would die. He indicated to us that he had no intention of changing his mind.

We referred him to the liaison psychiatrist for the hospital who independently assessed and found him to be competent and able to fully understand the implications of such a decision, i.e. his likely death from respiratory failure. The psychiatrist also found him to be depressed but noted that this did not interfere with his competence and ability to give or withhold his consent. With his consent, his family were informed of this development. They had been agonizing for some time over whether they had made the right decision to call emergency services when they first found him. They attempted to dissuade him but his resolve was unshakeable. Invasive ventilation was withdrawn on the morning of his 15th day of ITU as per his wishes. Diamorphine was administered to reduce symptoms of respiratory distress. He died of hypoxia later that day. Cause of death was recorded as aspiration pneumonia.

Describe the ethical and legal framework utilised in the management of this patient.Read More »

Thrombolysis in Pulmonary Embolism

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An elderly female was admitted under the care of the orthopaedic team with a 2 week history of decreased mobility due to right knee pain. She had a past medical history of chronic atrial fibrillation, treated with amiodarone, and asthma which was well controlled on salbutamol inhalers. She was not on warfarin. Bony injury was ruled out clinically and radiologically and she was treated with simple analgesia. Whilst on the ward, she deteriorated acutely after complaining of shortness of breath. A cardiac arrest call was put out.

On arrival of the cardiac arrest team, she had a cardiac output. On examination, she was hypotensive (BP 70/50 mmHg) with a heart rate of 55 bpm. She was markedly cyanosed with a respiratory rate of 30 breaths per minute with oxygen saturation of 75% on high flow oxygen through a reservoir bag. Her Glasgow Coma Score was 7 (E1V2M4). There was no evidence of calf swelling or tenderness. Arterial blood gas analysis revealed marked type 1 respiratory failure – pH 7.2, pO2 5.4kPa, pCO2 7.8kPa, HCO3 19mmol/l and lactate 4mmol/l .

She was rapidly intubated, and resuscitated with a total of four litres of crystalloids and colloids. Invasive blood pressure monitoring was established. A clinical diagnosis of acute pulmonary embolus was made. She remained unstable despite resuscitation, requiring frequent boluses of vasopressors and adrenaline thus being too unstable to be transferred for a CT pulmonary angiogram. A bedside echocardiogram showed a markedly dilated right heart with elevated right heart pressures. There was paradoxical movement of the interventricular septum. Left ventricular function was also slightly impaired.

It was decided to thrombolyse the patient. As alteplase was being readied, the patient arrested. The initial rhythm was pulseless electrical activity with a rate of 40 beats per minute. She was resuscitated as per Advanced Life Support (ALS) guidelines and received adrenaline and atropine intravenously. After two cycles of cardio-pulmonary resuscitation (CPR) and the administration of thrombolysis, she regained cardiac output but remained hypotensive and hypoxic. An adrenaline infusion was commenced through a peripheral line. Despite this, she arrested six further times with increasing inotropic support requirement. After two hours from the initial cardiac arrest call, the decision was made to stop resuscitation.

Post-mortem results confirmed the presence of a large pulmonary embolus as well as bilateral deep venous thromboses (DVTs).

What is the evidence for the use of thrombolysis in pulmonary embolism?Read More »

Metformin Associated Lactic Acidosis

Metformin Associated Lactic Acidosis

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A 65-year-old female, presented with epigastric pain and a 3-day history of diarrhoea and vomiting, dry mouth and breathlessness. She had also experienced a transient loss of vision three days earlier. Her past medical history included type 2 Diabetes, hypertension (on ramipril), hypothyroidism. On arrival, her GCS was 15/15. She was tachypnoeic (respiratory rate 31 breaths/minute) but maintained oxygen saturations at 98% on high-flow oxygen. On auscultation, she had bibasal crepitations.  She was tachycardic (irregularly irregular pulse of 130 beats/minute), had cool peripheries and dry mucous membranes. Her BP was 105/39mmHg. She had tenderness in her lower abdomen. Her initial arterial blood gas revealed a marked metabolic acidosis (pH <6.8, pO2 23.1, pCO2 1.9) with unrecordable bicarbonate and lactate levels. She was referred to the surgical and critical care teams with a working diagnosis of ischaemic bowel secondary to an embolic phenomenon (atrial fibrillation and possible amaurosis fugax).

She was resuscitated in ED with 4 litres of crystalloid but rapidly deteriorated, requiring vasopressor support to maintain her blood pressure. Her metabolic disturbance did not not correct with resuscitation and her lactate now registered as >15. Bloods showed Na 140, K+ 6.3, urea 35, Cr 1105. A decision to intubate was made in view of a deteriorating conscious level and need for urgent filtration and invasive monitoring. Noradrenaline (0.3mcg/kg/min) and dobutamine (26mcg/kg/min) were required to achieve a satisfactory blood pressure and she was commenced on CVVHDF. She was considered to unstable for transfer to CT or an emergency laparotomy. Her metabolic disturbance remained severe (pH<6.8 and lactate 13.9).

Within 24 hours her metabolic state had improved (pH 7.19, pO2 7.19, PCO2 2.5, HCO3 10, BE -28.1, Lac 6.7) and she became more cardiovascular stability. A CT effectively excluded an intra-abdominal catastrophe. Renal failure secondary to dehydration complicated by Metformin Associated Lactic Acidosis (MALA) appeared to be the most likely presentation. Her condition continue to stabilise and her vasopressor support and RRT was weaned over the next 7-10 days

What are the risk factors, clinical features and management of metformin associated lactic acidosis?Read More »

Management of Variceal Haemorrhage

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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.

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