Category: Basic Sciences

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 »

Albumin Use in Critical Illness

ICM Case Summaries2 Comments
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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Post Operative Cognitive Deficit after Cardiac Surgery

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A middle-aged  man underwent an elective re-do aortic arch replacement for a 6.1cm ascending aortic aneurysm distal to a pre-existing composite graft. Past medical history included a Bentall procedure (metallic aortic valve replacement, aortic root and ascending aorta replacement with coronary re-implantation into the composite graft) 20 years ago. Preoperative echocardiogram showed a well seated AVR and good biventricular function. Drug history included Warfarin (target INR 2-3) and Atenolol.

Anaesthetic induction and re-sternotomy were uneventful. Cerebral oximetry (rSO2) monitoring was utilized in this case. Cardiopulmonary bypass (CPB) was achieved uneventfully and deep hypothermic circulatory arrest (DHCA) was instituted. The patient was cooled to 18°C using CPB and icepacks. Prior to CPB and DHCA being commenced, intravenous thiopentone and methylprednisolone were administered for neuroprotection. Total DHCA time was 40 minutes and selective anterograde perfusion via the right axillary artery (chosen as it is relatively free of atheroma) was employed when rSO2 dropped to <40% and they remained >40% for the remainder of DHCA. Total CPB time was 105 minutes.

Following successful insertion of a new graft, the patient was carefully rewarmed to normothermia and weaned off CPB uneventfully, only requiring minimal vasopressor support. The patient was transferred to the cardiothoracic critical care unit.

After optimization of cardiorespiratory physiology, correcting coagulopathy and maintaining normothermia, with strict avoidance of hyperthermia, the patient was extubated the following day. For the first 48-72 hours postoperatively, delirium was the most active medical issues and this was managed according to conventional treatment. There was no focal upper or lower limb neurology. The patient did not require any other organ system support.

Following resolution of his delirium the patient was discharged to the ward to continue his rehabilitation. Prior to discharge, at approximately postoperative days 7-10, he was complaining of loss of short-term memory, reduced attention span and difficulty with finding words. A neurology review attributed this to cognitive dysfunction but no formal tests were carried out. A neurology clinic follow-up and an outpatient MRI scan were arranged.

What are the neurological complications after cardiac surgery?Read More »

Heparin Induced Thrombocytopaenia

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A 75 year old was admitted to the Cardiac Intensive Care Unit following aortic valve replacement for severe aortic stenosis. He had no other significant past medical history. He remained intubated and ventilated overnight until cardiovascularly stable, and was extubated the following morning. He suffered bleeding into the pericardial drains, and went back to theatre on day 3. He remained intubated on his return from theatre. On day 7 it was noticed that he had developed thrombocytopenia, with a platelet count of 34, reducing from 103 the previous day. A heparin induced thrombocytopenia (HIT) screen was sent, and he was changed to alternative anticoagulation.

The HIT screen was positive. His platelet count fell further and he continued to bleed slowly from any puncture sites and from around his mouth and gums. He remained intubated and ventilated and developed a requirement for inotropic support. Transfusions of platelets were required for any intervention. He was anticoagulated with lepirudin to prevent thrombosis. His platelet count continued to remain in single figures over the next 10 days despite treatment with steroids. Unfortunately he deteriorated, suffering an arterial thrombosis in his arm, renal failure and developed a necrotic skin rash all over his body, likely to be related to the HIT. Following discussions with his family, who felt he was suffering and would not want a poor quality of life, treatment was withdrawn on day 26 of his intensive care stay and she died.

What are the clinical implications of heparin-induced thrombocytopaenia?Read More »

Transplantation After Brainstem Death

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A 38-year-old previously fit man suffered a grade five subarachnoid haemorrhage. Attempts at coiling failed and he suffered a catastrophic rebleed on-table whereupon his pupils became fixed and dilated. After a suitable sedation washout period he underwent testing which confirmed brainstem death at which point he was referred to the specialist nurse for organ donation. Following counselling of the family and appropriate assessment, donation of his kidneys, liver and heart was agreed.

Upon confirmation of brainstem death, mechanical ventilation was continued to ensure PaO2 greater than 10 kPa and limit peak inflation pressure to less than 30 cmH20. Vasoactive support was switched from noradrenaline to vasopressin 0.02 iu/kg/min. Methylprednisolone and intravenous triiodothyronine were administered whilst awaiting harvest. Blood antibody testing for HIV1+2, Hepatitis B and C, HTLV-1 and CMV IgG were all negative. A transthoracic echocardiogram confirmed good biventricular function; following discussion with the transplant retrieval team a pulmonary artery catheter was floated. Clinical measurements of cardiac output and mixed venous oxygen saturation were satisfactory. Adequate hydration was maintained with crystalloid by infusion and glucose control optimised in the range 8-10 mmol/L with insulin. The dedicated retrieval team performed the organ retrieval eighteen hours after confirmation of brainstem death.

How can we optimise organ function for organ donation?Read More »

Refractory Status Epilepticus

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A middle aged man presented with seizures. For 4 days he had been feeling unwell with coryzal symptoms, frontal headache and dizziness. He had ‘not been himself’ for some months. He had no previous medical history and had never had a seizure before. The ambulance crew noted that he was confused and witnessed a generalised tonic-clonic seizure. On arrival in hospital he was severely agitated and uncooperative and received IV lorazepam.

He was not adequately protecting his airway, saturations were 100% on high flow oxygen, temperature was 37.8, his pulse was 88, BP 129/90mmHg, blood sugar was 7.7. Clinical examination did not reveal any abnormality except for diminished level of consciousness. A presumptive diagnosis of meningitis / encephalitis was made. His trachea was intubated, he received fluids, parenteral vitamins, IV ceftriaxone and acyclovir. A CT head (with contrast) was obtained and a lumbar puncture were normal. His blood tests, CXR, urinary toxicology screen, and ECG were non-contributory. Arterial blood gas analysis revealed changes consistent with being post ictal and then (whilst ventilated) normalised.

His sedation was weaned and once extubated he remained very drowsy, even 18 hours after his last sedation. A Glasgow Coma Score (GCS) was recorded at E1V1M5 (7/15). His pupils were equal and reactive, and he was moving all 4 limbs. Both plantar responses were down-going, and tone and reflexes were symmetrical. He had myoclonic jerking of his left hand but no rhythmical muscle activity was evident. To protect his airway he required reintubation of his trachea and re-institution of ventilation.

In addition to sedation with propofol and alfentanil he received therapeutic phenytoin. An electroencephalogram (EEG) performed on his second day, off sedation, revealed continuous periodic sharp and slow wave complexes at around 1Hz with intermittent high amplitude waves in the left temporal region and bursts of rhythmical activity in the right temporal region. At the time of the EEG he had some abnormal motor activity – continuous movement of his fingers and twitching of an eyelid and rhythmical jerking of both of his arms. An MRI of his brain was normal.

In this clinical context the EEG was interpreted as being consistent with encephalitis and non-convulsive status epilepticus.  Phenobarbitone was started in addition to the phenytoin. Normothermia and normoglycemia was maintained. To improve the management of his non convulsive status we continuously monitored his cerebral electrical activity with a bispectral index (BIS) monitor and bitemporal EEGs. We targeted a burst suppression of 20-50%. Propofol was ineffective at reducing the BIS without causing limiting hypotension but midazolam was effective.

Further investigations did not further our search for the primary diagnosis. A further EEG was performed 24 hours later, off midazolam but whilst on 350mg/hr of propofol. He developed some rhythmical motor activity and his EEG revealed ongoing abnormal electric activity, consistent with continued non-convulsive status, which resolved in response to a bolus of propofol. A possible diagnosis of limbic encephalitis was considered and methylprednisolone (1g IV) was administered.

A repeat MRI showed increased abnormal signal changes in the amygdala and hippocampus, which is supportive of the diagnosis of limbic encephalitis.

Despite optimal medical treatment his EEG showed more severe and continued abnormal electrical activity. Thiopentone was added to his anti-seizure regime. By the 19th day from initial presentation multiorgan failure had developed. He required ventilation with high airway pressures and high inspired oxygen concentrations for lung injury due to ventilator associated pneumonia, vasoactive drugs to support his cardiovascular system through the associated sepsis, haemofiltration for renal failure and had ileus with failure of enteral feeding. There were still signs of seizure activity despite concurrent administration of propofol, midazolam, phenytoin, levetiracetam, phenobarbitone and sodium valproate. Supportive treatment was withdrawn following diagnosis of brain-stem death. His family did not permit a post mortem examination.Read More »

Use of Bicarbonate in Lactic Acidosis

Steve Mathieu3 Comments

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

ICM Case Summaries1 Comment

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 »

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 »