Author: ICM Case Summaries

High Frequency Oscillatory Ventilation in ARDS

High Frequency Oscillatory Ventilation in ARDS

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A 45 year old female presented to A&E with a 5 day history of worsening SOB, cough productive of green sputum, lethargy, anorexia, fever and rigors. She had no co- morbidities and was active and independent with a good exercise tolerance. On examination she looked unwell, clammy and drowsy. Her respiratory rate was 35 breaths per minute and SpO2 of 84% on 15 Litres of oxygen via a non-rebreathing mask. Her blood pressure was 88/40 mmHg with a heart rate of 140 per minute despite having received 3 litres of fluid. Arterial blood gas showed PaO2 6.0kPa, pH 7.28, PaCO2 7.1 kPa, Bicarbonate 14 mmol/l, BE -11 and Lactate 8.6 mmol/l. Chest radiograph demonstrated significant bilateral consolidation with infiltrates consistent with ARDS. PaO2:FiO2 was calculated as 15 indicating severe ARDS presumed secondary to CAP.

She was managed as per sepsis guidelines. Oxygen therapy was continued and CPAP was initiated due to the hypoxia whilst an ICU bed was being prepared for admission. Noradrenaline was commenced at 0.2mcg/kg/min which continued to increase. Repeat arterial blood gases confirmed worsening type 2 respiratory failure and the patient was clinically exhausted. A modified rapid sequence induction was performed and IPPV commenced. Her oxygenation remained a problem and despite a FiO2 of 1.0 and PEEP of 20 his SpO2 remained 85% and PaO2 6kPa. The patients’ sedation was deepened and muscle relaxant administered. Lung protective ventilation was continued however arterial blood gases continued to worsen. The decision was made to convert the patient from conventional ventilation (CV) to High-Frequency Oscillator Ventilation (HFOV). The initial ABGs after an hour of HFOV showed an improvement as did subsequent numbers. This mode of ventilation was continued for a further 48 hours and then converted to CV. Gas exchange continued to improve. Over the course of the following 4 weeks the patient had a tracheostomy performed to aid weaning. She subsequently developed a Ventilator Associated Pneumonia and worsening ARDS required a further period of HFOV. Improvement continued and the patient was successfully decannulated and discharged from ICU.

What is the evidence base for high frequency oscillatory ventilation in ARDS?

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Secondary Complications of Subarachnoid Haemorrhage

Secondary Complications of Subarachnoid Haemorrhage

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A thirty eight year old female smoker was admitted via A+E following sudden onset occipital headache with visual disturbance and collapse with loss of consciousness lasting approximately five minutes. She had complained of unusual headaches a week prior to this event, but these were short lived and not associated with any neurology. On arrival in resus she had recovered to a Glasgow coma score (GCS) of 14/15. She demonstrated neck stiffness and photophobia, as well as general irritability. Plain computerised tomography
scan (CT) performed showed a subarachnoid haemorrage in the region of the middle cerebral artery, with the presence of blood in the sylvian fissure.

She was transferred to the ITU for monitoring and blood pressure control with invasive arterial and central venous pressure monitoring. She was treated with nimodipine to prevent vasospasm. Contrast CT performed showed an aneurysm at the bifurcation of the middle cerebral artery, and this was felt to be the origin of the bleed. She underwent uneventful endovascular coiling of this aneurysm the following day under general anesthesia, and was discharged to the neurosurgical team for ongoing care afterwards.

What are the secondary complications of subarachnoid haemorrhage and how are they managed?

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Steroids in Cervical Spine Injury

Steroids in Cervical Spine Injury

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A previously fit and well 46 year-old was admitted via the emergency department having sustained a neck injury whilst horse riding. She was unable to move her arms and legs immediately after the fall. On arrival to the Emergency Department, she was alert and orientated. Examination of the cardiovascular and respiratory system was unremarkable although there was evidence of diaphragmatic breathing.

Examination of her neurological system revealed:

•A sensory level at C6
•Absent upper limb reflexes except for brisk bicep reflex bilaterally
•⅖ power in shoulder abductors bilaterally
•Flaccid paralysis of her lower limbs
•No anal tone

She was initially managed in a hard neck collar with full spinal immobilisation. CT brain was reported to be normal. CT neck showed an obviously displaced fracture of C5 and C6 vertebral bodies. She was transferred to the intensive care unit for cardiovascular, respiratory and neurological monitoring while a definitive treatment plan was being considered. After discussions with the orthopaedic surgeons, it was decided not to commence high-dose steroids. This decision was reinforced after discussion with the local neurosurgical and spinal units. It was also decided not to surgically stabilise the c-spine due to the higher risk of respiratory complications. She was transferred to the spinal rehabilitation unit after 2 days.

What is the role of steroids in cervical spine injury?Read More »

Ethylene Glycol Poisoning

Ethylene Glycol Poisoning

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A 50 year old man was found by the roadside by paramedics with a GCS of 13. On arrival he had a patent airway, but a GCS of 5 (E1 M3 V1). He had an elevated respiratory rate (30/min) and a profound metabolic acidosis (pH 6.97 pO2 16.8 pCO2 1.68 HCO3 2.8 BXS -30.8 COHb 0). The lactate was too high to be measured by the blood gas analyser and there was an elevated anion gap [(147+5.5) – (2.8+ 109) = 40.7] He was cardiovascularly stable with warm peripheries. His ECG revealed a prolonged QTc. He was intubated and 8.4% sodium bicarbonate was administered. His initial laboratory bloods showed CRP 11, white cell count 29.5 CK 2539 creatinine 213. Ethanol levels were <10 and Paracetamol and salicylate levels were within normal limits. He was given a dose of intravenous cefotaxime and his urine was sent for organic acids screening which revealed an enormous peak of glycolic acid and small increase in oxalic acid, consistent with an overdose of ethylene glycol.

After arrival in intensive care, the sodium bicarbonate had improved the pH to 7.2, with a residual lactaemia (15 as measured in the laboratory, without any interference from glycolic acid). CVVHDF was commenced. In order to inhibit futher metabolism of the ethylene glycol, 10% ethanol was commenced until fomepizole was available (an initial bolus of 800ml, followed by an infusion at 180ml/hr). Ethanol levels were monitored. Fomepizole was administered later that day abd the ethanol stopped (15mg/kg loading and 1mg/kg/hr). The renal function deteriorated despite CVVHDF (peaked at urea 28, creatinine 724 on day 4), which was continued for 5 days. Treatment for aspiration pneumonia was started in day 1 and cardiovascular support was continued (noradrenaline). Intermittent boluses of glycopyrolate were required to treat the bradycardia associated with fomepizole. A gradual improvement occurred and he had made a full neurological recovery within 2 weeks, with much improved renal function. He later admitted to drinking 250ml of antifreeze.

What are the clinical features and management of ethylene glycol poisoning?Read More »

Glutamine in Critical Illness

Glutamine in Critical Illness

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A forty-year-old motorcyclist was admitted to the ITU following a road traffic accident involving a stationary vehicle. She sustained a fractured right distal radius and multiple left sided rib fractures, involving ribs 2 to 9, with a free floating flail segment. She developed respiratory distress due to underlying lung contusions and a haemopneumothorax and was treated with two left sided intercostal drains, endotracheal intubation and invasive ventilation. She developed ARDS with bilateral infiltrates and PF ratio of <200mmHg, with normal cardiac function on transthoracic echocardiography. She was tracheostomised on day 12, and had a protracted ventilatory wean further complicated by a ventilator associated pneumonia. She was enterally fed during this period but began to develop an ileus and gut dysmotility, resistant to prokinetic treatment, leading to large volume gastric aspirates. She became visibly malnourished and was commenced temporarily on parenteral nutrition and IV glutamine. The ileus resolved over the following week and weaning recommenced, having ceased due to diaphragmatic splinting. She eventually weaned from the ventilator and was discharged from the ITU on day 40. She was profoundly weak due to a critical illness acquired weakness.

What is the role of glutamine supplementation in critical illness?Read More »

Obesity Hypoventilation Syndrome

Obesity Hypoventilation Syndrome

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 A 66 year old man was brought by ambulance to ED after becoming acutely dyspnoeic at home, and his wife had struggled to wake him after an afternoon sleep. He had a moderate smoking history of 20 pack years and quit 20 years ago, and drank approximately 20 units of alcohol as beer per week. There were no preceding prodromal respiratory or infective symptoms reported. On examination, he was obese with a weight of 120 kg. He was snoring, which eased with a chin-lift or jaw thrust, but he would not tolerate an airway adjunct. His respiratory rate was 8 and shallow, producing SpO2 84% on high flow oxygen. He was flushed and veno-dilated peripherally, with a tachycardia of 110 bpm sinus rhythm. Most notably, he was difficult to rouse, with a GCS of 9 (E2 M5 V2). Arterial blood sampling revealed a profound hypercapnoeic respiratory acidosis with no degree of compensation. Chest X-ray showed poorly expanded lungs with bilateral basal atelectasis and prominent pulmonary vasculature. Empiric naloxone was ineffective and he was commenced on non-invasive ventilation (NIV). The working diagnosis was an acute non-infective exacerbation of previously undiagnosed chronic obstructive pulmonary disease (COPD). Treatment involved bronchodilators, steroids and bilevel pressure support non- invasive ventilation.
One hour after NIV had been established, the patient’s respiratory acidosis was worse and his clinical picture was unchanged. He was intubated then transferred to Intensive Care. CTPA ruled out significant pulmonary emboli but was suggestive of pulmonary hypertension. Ventilation was not difficult, with near normal inspiratory pressures, and his minimal wheeze resolved quickly. As his respiratory acidosis normalised, his GCS rapidly improved to the point of safe extubation after just 48 hours. Given his obesity he was extubated to non-invasive pressure support ventilation immediately. After a further 24 hours, his gas exchange began to deteriorate again. Increasing inspiratory pressure improved his tidal volumes but his intrinsic rate of breathing slowed such that his minute ventilation remained static. He eventually found a stable equilibrium using nocturnal bilevel pressure support with a high mandatory backup rate (pressure control), which maintained a normal minute ventilation. Although he developed hypercapnoea each night, this was mild and eventually compensated. With the NIV, he did not obstruct, have hypopnoeic events or desaturated overnight, which markedly improved his daytime somnolence and effort of breathing.

What are the clinical features and approaches to management of obesity hypoventilation syndrome?

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Scoring Systems for Acute Hepatic Dysfunction

Scoring Systems for Acute Hepatic Dysfunction

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A 40 year old was admitted to hospital with his first presentation of alcoholic liver disease with symptoms of jaundice (bilirubin 248), poor mobility, hallucinations and passing of black stool. On admission to hospital, he was lethargic with features of Grade II encephalopathy, was coagulopathic (INR 3.1), had deranged electrolytes (sodium 114, potassium 2.9), but a normal creatinine (54) and a raised white cell count (15.9). He was haemodynamically stable and had a haemoglobin of 119g/L with no signs of active bleeding. His abdomen was distended (ascites), he was visibly jaundiced and had spider naevi on his chest. An abdominal ultrasound was performed that showed liver cirrhosis, borderline splenomegaly, small volume ascites and normal kidneys. A full liver screen revealed no infective cause and his AST:ALT ratio suggested alcoholic liver disease. His prognostic indicator scores were all suggestive of severe alcoholic liver hepatitis (Maddrey score: 131; Childs: C; Lille Score: 1; GAHS: 10; MELD: 29). His serum ammonia level was 170. He was commenced on terlipressin, prednisolone and pentoxyphylline and thiamine. Despite this, his encephalopathy progressed to grade 4 and he required intubation and ventilation for airway protection and a presumed aspiration pneumonia. His liver function and coagulopathy continued to worsen, and he developed an acute kidney injury necessitating commencement of renal replacement therapy. He required noradrenaline to support his blood pressure. Ascitic tap ruled out spontaneous bacterial peritonitis. He was discussed with regional liver centres, but was not felt to be a transplant candidate. His liver and renal function continued to deteriorate and eventually treatment was withdrawn nearly 3 weeks into his admission.

Describe the scoring systems for assessing the severity of acute hepatic dysfunction.

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Coiling versus Clipping Subarachnoid Haemorrhages

Coiling versus Clipping Subarachnoid Haemorrhages

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A 40 year old female presented with a severe sudden onset headache, and deteriorated in the emergency department with worsening agitation and confusion requiring intubation and ventilation for her own safety. A CT scan diagnosed a Fisher Grade 4 subarachnoid haemorrhage and obstructive hydrocephalus. Clinical presentation was scored as Hunt and Hess grade 4 or World Federation of Neurosurgeons grade 4. The patient was transferred to the local tertiary Neurocritical care unit where an extra-ventricular drain was inserted overnight. The following day the patient underwent coiling of her right middle cerebral artery aneurysm in the radiology suite. A Magnesium infusion and Nimodipine therapy were commenced to reduce the risk of vasospasm. On initial sedation hold she woke up agitated so she had an early tracheostomy placed to allow controlled wake up. She had a straightforward respiratory wean from the ventilator over the next few days. Neurological recovery was good (Glasgow coma score improved to 14/15) and the patient was discharged to the ward for on-going neuro rehabilitation and repatriation to the base hospital.

What are the risks of clipping vs coiling subarachnoid haemorrhages?Read More »

Guillain-Barré Syndrome

Guillain-Barré Syndrome

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A sixty year old man was admitted to the ITU with respiratory failure. He initially presented with a week long history of limb weakness that started in his legs. CSF sampling showed elevated protein levels and a diagnosis of Guillain-Barré Syndrome (GBS) was made. Symptoms progressed to weakness in coughing and deep breathing. Serial vital capacity measurements progressively deteriorated. His vital capacity on referral to ITU was 1.2L (roughly 15ml/kg), he was having difficulty expectorating and had an acute respiratory acidosis with hypercapnia. Treatment was commenced with intravenous immunoglobulin. He was initially treated with non-invasive ventilation but he continued to deteriorate largely because of sputum retention. He was sedated, intubated and invasively ventilated and after 7 days he underwent percutaneous tracheostomy to facilitate bronchial toilet and weaning. His respiratory function improved slowly and he was decannulated after 22 days of invasive ventilation. He was discharged back to neurology services for rehabilitation after a further 9 days on ITU. He remained profoundly weak on discharge and was unable to mobilise or transfer without assistance.

What are the clinical features of Guillain-Barré Syndrome and how is it managed on the ICU?
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Rapid Response Systems

Rapid Response Systems

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An elderly man was admitted with an acute abdomen and free air visible under the diaphragm on CXR. He was fluid resuscitated before undergoing emergency laparotomy, where a perforated duodenal ulcer was oversewn. He was admitted to ICU postoperatively, extubated the next morning and deemed fit for discharge to the surgical ward later that day. Due to a lack of surgical beds, he was eventually discharged from ICU at 22:30. Eight hours post discharge, he was urgently re-referred to ICU after being found moribund on the ward. Before he could be seen and assessed he suffered an unrecoverable asystolic arrest. Review of his observation charts showed that there had been a clear deterioration in recorded observations, including hypotension for the two preceeding hours. However, the Early Warning Score had been calculated incorrectly, and no escalation had occurred.

What evidence is there that rapid response systems are effective in preventing patient deterioration and improving outcomes?

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