Category: Physiology & Biochemistry

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 »

Invasive Ventilation of Life-Threatening Asthma

Invasive Ventilation in Life-Threatening Asthma

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An 18-year-old known asthmatic presented with a two-day history of increasing shortness of breath on a background of a recent coryzal illness. She had a background of reasonably poor control and had been admitted to the intensive care unit for mechanical ventilation twice as a child. Her current medication included regular inhaled serotide 250, montelukast 10mg and theophylline MR 450mg BD. At presentation she was in extremis; pulse rate was 65 per minute, blood pressure 75/54 mmHg and respiratory rate 14 per minute. Arterial blood gas analysis demonstrated a PaCO2 of 11 kPa and PaO2 of 7.6 kPa with associated respiratory acidosis. Nebulised salbutamol and intravenous magnesium sulphate therapy was administered. along with 200mg of intravenous hydrocortisone. On arrival of the intensive care team, the patient’s respiratory rate deteriorated to a rate of 4 per minute. Assisted ventilation with a self-inflating bag and 100% oxygen was performed; rapid-sequence intubation was performed using ketamine and rocuronium.

Following intubation, immediate difficulties were experienced with mechanical ventilation. High airway pressures in excess of 40 cmH2O with tidal volumes of less than 200 ml were observed. Immediate chest radiography confirmed correct positioning of the endotracheal tube and excluded a pneumothorax. Adequate sedation and neuromuscular blockade were confirmed. Auscultation confirmed severe, widespread wheeze with limited air entry. Further nebulised salbutamol was administered and an aminophylline infusion initiated. The patient was transferred to the intensive care unit where magnesium, ketamine and vecuronium by infusion were added. Various modes of mechanical ventilation were tried including volume and pressure triggered with varying success; this included lengthening the I:E ratio, frequent disconnections to allow deflation and adjustment of PEEP to maximum compliance. Continuous salbutamol was administered via an ultrasonic nebuliser. Airway pressures remained high and there was little improvement in her acidosis. 2 hours after admission the patient suffered a PEA cardiac arrest from which she could not be resuscitated.

What are the difficulties in ventilating severe asthmatics, and what strategies can we use to overcome them?

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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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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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When to Initiate Parenteral Nutrition

When to Initiate Parenteral Nutrition

Steve Mathieu2 Comments

A 19 year old man presented to the surgical team complaining of abdominal pain. He underwent a laparoscopic appendicectomy and a perforated appendix was removed. He returned to the surgical ward and three days later was ready for discharge. Unfortunately he then developed worsening abdominal pain, fevers and breathlessness. He underwent a CT scan and this demonstrated multiple collections of infected matter within his abdomen in addition to bi-basal atelectasis. He was admitted to the intensive care unit for haemodynamic monitoring, oxygen therapy and broad spectrum antibiotics. He underwent three intra-abdominal washouts of infected material over an eight day admission. During this time he had attempted enteral feeding via a nasogastric tube but had very high gastric aspirates, with no absorption, as a result of a prolonged ileus. He was started on parenteral nutrition on day eight of his ICU admission.

When should parenteral nutrition be initiated in those that are failing to meet caloric targets with enteral feeding alone?

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Lactate Physiology and Predicting Disease Severity

Lactate Physiology and Predicting Disease Severity

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A middle aged man presented with urosepsis after several days antibiotic therapy in the community. He was in septic shock, with tachypnoea, tachycardia and hypotension. He had raised inflammatory markers and acute kidney injury. His initial lactate level was 14mmol/L with a significant metabolic acidosis (base deficit 21). He was commenced on iv antibiotics, noradrenaline and renal replacement therapy. Lactate levels cleared to less than 2mmol/L over the next 24hrs. He weaned off noradrenaline in 72 hours and CVVHDF over the next 5 days.

How is lactate produced and what is its significance in predicting the severity of critical illness?

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Medical Management of Abdominal Compartment Syndrome

Medical Management of Abdominal Compartment Syndrome

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An elderly man was admitted after a Hartman’s procedure with primary closure for a perforated sigmoid diverticulum with four quadrant peritonitis. Postoperatively, he remained ventilated and noradrenaline dependent. His intra-abdominal pressures gradually rose from 15 to 24mmHg. Urine output was poor, and he required peak pressures of 28cmH2O to achieve 6ml/kg tidal volumes. Vasopressor requirements gradually increased and a diagnosis of abdominal compartment syndrome was made. Medical management was attempted with fluid resuscitation, increased sedation, aspiration of nasogastric tube and neuromuscular blockade. However this did not improve the intra-abdominal pressures so the patient returned to theatre laparostomy and VAC dressing. On return from theatre, intra-abdominal pressures stabilised between 12 and 15mmHg. Noradrenaline requirements fell and urine output improved. The abdomen was closed on day 5 and he was discharged from ICU on day 10.

What non-surgical strategies can be used to reduce intra-abdominal pressure?

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