Category: Case Summary

Hyponatraemia and Renal Replacement Therapy

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A 63 year old woman was admitted to the ICU from the Emergency Department with acute alcohol withdrawal, severe hyponatraemia (serum sodium level 114mmol/L), rhabdomyolysis (creatine kinase 46930u/L) and acute kidney injury (serum creatinine 262umol/L, urea 8.7mmol/L, potassium 4.6mmol/L, base excess -6.8 and anuric from the point of admission). Her corrected calcium level was 1.92mmol/L. She had been discovered on the floor at home after a presumed fall. It was unknown how long she had been on the floor, but there were extensive pressure injuries to the left elbow, buttocks and left leg. A CT scan of the brain had excluded significant acute intracranial pathology and a 12 lead ECG showed atrial fibrillation at a rate of 130 beats per minute.

The patient was intubated and mechanically ventilated to allow emergency treatment. She was sedated with remifentanil and propofol. Intravenous pabrinex and enteral chlordiazepoxide was given to treat her alcohol withdrawal, aiming for early extubation if possible. A low-dose noradrenaline infusion was required to maintain a mean arterial pressure ≥65mmHg. Calcium replacement was prescribed and full pressure relief measures were instituted. No specific treatment was given to rate control or cardiovert the patient.

The patient was clinically hypovolaemic, but since the duration of hyponatraemia was unknown (with suspicion of some chronicity related to alcohol dependence), aggressive fluid resuscitation was avoided. Continuous veno-veno haemodiafiltration (CVVHDF) was commenced using standard replacement fluid at a post-filter replacement rate of 10ml/kg/hr-1 and dialysate flow rate of 10ml/kg/hr-1 (blood pump at 200ml/hr). Concomitantly, a 5% dextrose infusion was administered; the rate of infusion and net fluid loss through ultrafiltration were adjusted constantly with a view to restoring euvolaemia over 24 hours while increasing serum sodium to a maximum level of 120mmol/L over the same time period. This strategy was continued the following day with a target sodium of 128mmol/L, thereafter tight control of sodium correction was relaxed.

She was extubated on day 3 and renal replacement was discontinued on day 4. The patient was discharged from ICU on day 6. At the point of discharge her serum sodium concentration was stable at 142mmol/L. She was neurologically intact.

What are the challenges in managing hyponatraemia in critically ill patients?Read More »

Massive Propranolol Overdose

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A 35 year old male presented with massive (over 1500mg) propranolol overdose on a background of depression and anxiety. He called for help and was found alert and cardiovascularly stable by paramedics at 50 minutes post ingestion. By 80 minutes his conscious level had fallen to a Glasgow Coma Score of 11 and he had become hypotensive. He started fitting en route to hospital and lost cardiac output as he arrived at hospital. The initial cardiac arrest rhythm was broad complex slow pulseless electrical activity. After a prolonged resuscitation attempt he regained spontaneous cardiac output but never achieved cardiovascular stability and sadly died later that evening.

He was resuscitated according to standard resuscitation algorithms. In addition, several specific therapies were given in line with Toxbase recommendations1: Glucagon was administered as a 10mg slow bolus followed by a 100-150 mcg/kg/hr infusion. Insulin (actrapid) was given as a 60 unit bolus followed by a 1-2 unit/kg/hr infusion along with a glucose bolus of 0.5 g/kg followed by an infusion of 0.5 g/kg/hr. Intralipid was delivered as a bolus (100 ml 20%) followed by an infusion. Atropine 3mg was given and the adrenaline boluses were changed to an infusion at 10 mg/hr.

Cardiac arrest remained refractory until a 100 ml bolus of 8.4% Sodium Bicarbonate was administered prompting almost instantaneous restoration of circulation.

The circulation remained unstable with a broad complex bradycardia resistant to transcutaneous pacing. High dose adrenaline infusion, high dose euglycaemic insulin therapy and glucagon infusion were continued. Transvenous pacing was also ineffective and the patient sadly deteriorated into a refractory cardiac arrest from which he did not recover.

The patient regained his cardiac output when the sodium bicarbonate bolus was given. The temporal association between these two events was profound and led me to question why this therapy sits so far down the toxbase treatment algorithm.1

This case summary aims to answer: 

  1. What works in Propranolol overdose? 
  2. What doesn’t really work? 
  3. Which order should I give things?

Read More »

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 »

Invasive Fungal Infections on ICU

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A 42 year old woman was admitted to the intensive care unit with necrotising pancreatitis. She required sedation and mechanical, vasopressors to maintain adequate mean arterial pressure and extensive crystalloid resuscitation. Enteral nutrition was initially maintained via nasogastric feeding. She was treated with empirical broad-spectrum antibiotics (meropenem) and was prescribed antifungal prophylaxis (fluconazole) at the request of the hepatobiliary surgical team.

 

The patient experienced a prolonged systemic inflammatory response syndrome. She ultimately underwent a pancreatic necrosectomy and required recurrent radiologically-guided percutaneous drainage of intra-abdominal collections. For a large proportion of her ICU admission, enteral nutrition failed and the patient required total parenteral nutrition. Candida albicans was isolated from central venous catheter exits sites, drain exit sites, drain fluid, urine and sputum on several occasions, but there was never any evidence of invasive fungal disease.

The patient was eventually discharged from ICU and survived to discharge from hospital. She was left dependent on pancreatic enzyme replacement and subcutaneous insulin therapy.

Describe the incidence, clinical features and management of fungal infections in non-neutropaenic, non-transplant critical care patients.Read More »

Graft versus Host Disease

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A 34-year-old woman received a small bowel, pancreas and abdominal wall transplant.

Despite the operation being technically very difficult and prolonged, she initially recovered well after the procedure and her transplanted bowel started to work. However, after a few days she started developing respiratory complications eventually requiring re-intubation despite antibiotics. She went on to develop multi-organ dysfunction requiring vasopressor support and renal replacement therapy. Antifungals and co-trimoxazole were added, with no additional benefit noted.

A skin rash started to develop, which raised the suspicion of Graft versus Host Disease (GvHD). A diagnostic test was performed (chimerism of peripheral blood leucocytes), and it confirmed the diagnosis of GvHD.

Doses of immunosuppressants such as tacrolimus, mycophenolate mofetil were increased and steroids were started too.

An experimental therapy of mesenchymal stem cells infusion was also employed, but she continued to deteriorate further and she eventually died after a prolonged admission on ICU.

Graft versus Host Disease – what it is, how to diagnose it, how to treat itRead More »

Extracorporeal CO2 removal

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A 42 year old man presented with a week-long history of increasing shortness of breath, cough  (productive of purulent sputum) and fevers on a background of significant chronic lung disease. He had a ten year history of interstitial lung disease and was on the waiting list for a lung transplant. He used oxygen at a rate of 2 litres per minute at home, 24 hours a day. His usual exercise tolerance of 200 metres had been significantly reduced for the past week. His regular medications included seretide and salbutamol inhalers, lansoprazole, azathioprine, prednisolone alendronate.

On arrival in hospital, he was alert and orientated. He had a patent airway, but was tachypnoeic (rate of 50/minute) using his respiratory accessory muscles and a tracheal tug was evident. An arterial blood gas revealed type two respiratory failure (pH 7.26; pO2 8.14, pCO2 7.52 on 15 liters/min of face mask oxygen). He was hypotensive (80/40mmHg) and tachycardic (130/minute, sinus rhythm). A pyrexia of 39.2°C was recorded. Blood results showed normal renal function, a slightly elevated white cell count of 14.

The patient was admitted to the high dependency for close monitoring in view of his history and presentation. He was commenced on treatment for a presumed infection (viral or bacterial) with oseltamivir, co-amoxiclav and clarithromycin and given three “pulsed” doses (750mg) of methylprednisolone. He remained stable for the next twelve hours.

Early the next morning, he became very hypoxic (oxygen saturations less than 50%), bradycardic (<35 beats per minute) and had a brief hypoxic respiratory arrest. He received 1 cycle of cardiopulmonary resuscitation and was intubated. There was subsequently a return of spontaneous circulation.

The next 24 hours involved a period of difficulty with ventilation. His peak airway pressures were very high, despite being paralysed and a low volume/high respiratory rate strategy being employed. He was discussed with a tertiary respiratory centre and it was decided that he should be transferred for insertion of a pumpless arteriovenous interventional lung assist (for extracorporeal carbon dioxide removal) as a bridge prior to lung transplantation. He had formal ultrasound measurement of his femoral arteries. His left common femoral artery was widely patent (AP and transverse diameter of 8-9mm throughout), but the right was only 4-5mm throughout.

In the meantime, his peak airway pressures were consistently between 35 and 40cmH2O, despite tidal volumes of 230ml, 3.8ml/kg). With a rate of 32-35 breaths per minute, his pH was  initially maintained above 7.2, with a pCO2 of 9-11kPa. Over the course of the next few hours, this became increasingly difficult to achieve. His oxygen requirements did not escalate (an FiO2 of 0.6 provided a pO2 of 8-9kPa). When his pCO2 increased to 15.4kPa and his pH dropped to 7.17, further adjustments were made and the PEEP decreased to 5cmH2O from 10cmH2O. His noradrenaline requirements were increasing and with the aid of the cardiac output monitoring, he was cautiously given fluid with a good response.

He was transferred to the centre in which a lung transplant could be performed within hours of the referral. A Novalung device was inserted and he underwent a bilateral lobar lung transplant several days later. He was in hospital for 6 weeks and made a very good long-term recovery. At six months, he was extremely well and was undertaking his activities of daily living completely normally with stable lung function. He even managed to complete an eight mile bike ride.

What is the rationale for extracorporeal lung assist?
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Faecal Peritonitis: The Role of Laparostomy

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A 68-year-old previously fit woman was admitted with left lower abdominal pain and signs of cardiovascular shock. She had had a 2 day history of crampy left lower abdominal pain and altered bowel habit. Clinically she had a diagnosis of bowel perforation with generalised peritonitis. She was exhibiting signs of shock with a pronounced tachycardia and a reduced systolic blood pressure.

She was started on fluid resuscitation and intravenous antibiotics. After her cardiovascular system stabilised she was taken to the operating theatre where she had a laparotomy. A sigmoid perforation was found with four quadrant faecal contamination. A Hartmann’s procedure was performed. A laparostomy was decided upon at the first instance, and was covered with a VAC dressing.

She was transferred to the intensive care unit (ICU) still intubated and ventilated.

Her condition rapidly worsened on the ICU. She required vasopressor support intra-operatively and her requirements rapidly escalated. She seemed to stabilse over the next 36 hours. Her condition then worsened and she was taken back to theatre for a washout of her peritoneal cavity. A number of collections were found and further soiling of her abdomen was evident. Her condition remained the same for the next 12 hours but then started to show an improvement again. She continued to make a good response to treatment over the next 3-4 days. She had another washout at 4 days. She was extubated on day 5 and invasive monitoring and cardiovascular support was no longer needed.

 

What is the role of laparotomy in the management of faecal peritonitis?Read More »

Thrombotic Thrombocytopaenic Purpura

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A previously fit and well 64 year old gentleman presented to the acute medical unit with a two-week history of lethargy, bruising, dark urine and an episode of transient facial numbness, blurred vision and dysarthria lasting 30 minutes. Clinical examination revealed mild jaundice, multiple bruises and a palpable liver edge but was otherwise normal. His respiratory rate was 14 breaths/minute with normal oxygen saturations. He was in sinus rhythm with a pulse of 68 beats/minute and non-invasive blood pressure was 130/70. He was GCS 15 and was apyrexial.

His full blood count revealed a haemoglobin of 94 g/L, platelets 9 x109/L, and white cell count 9 x109/L. A blood film showed red cell fragmentation, spherocytes, polychromasia, poikilocytosis and no platelet clumps. Reticulocytes and lactate dehydrogenase were raised at 168.6 x 109/L and 3027 iu/L respectively. Liver function tests revealed a bilirubin of 49 µmol/L but were otherwise normal. A liver ultrasound showed fatty infiltration. Clotting was normal and direct antiglobulin test negative. Urea and electrolytes were normal, creatinine 80 µmol/L and the C reactive protein was 37. ADAMTS13 assay showed complete absence of activity. CT brain was normal.

He was reviewed by the haematologists who diagnosed thrombotic thrombocytopenic purpura and referred him to the intensive care unit for plasma exchange. He received a three-day course of methylprednisolone, was intubated due to agitation, received plasma exchange with octaplas replacement that increased from 2 litre to 5 litre exchanges, and rituximab 750mg.

He deteriorated progressively with: vomiting, anaemia requiring blood transfusions, worsening thrombocytopenia, acute kidney injury with a peak creatinine of 457 µmol/L, an inferior ST elevation myocardial infarction, and a posterior cerebral artery territory infarct.

On day 5 he developed fixed and dilated pupils. Mannitol 1g/kg was administered and an urgent CT brain performed. This revealed multiple infarcts in both cerebral hemispheres and right cerebellum, loss of grey-white differentiation, 5mm midline shift and low cerebellar tonsils.

After discussion with the neurosurgeons it was decided this was an unrecoverable injury. In agreement with his family, end of life care was instituted and he died within 24 hours.

Describe the management of Thrombotic Thrombocytopaenic Purpura.Read More »

Declining Admission to Intensive Care

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An 86 year-old man was referred to ICU because of oliguria, acidaemia and decreased conscious level. He had originally been referred by the general practitioner to the acute general medicine team with unexplained weight loss, malaise and reduced mobility, 19 days previously. He had a longstanding history of bronchiectasis and COPD. He had been able to mobilise independently around his house and garden until suffering a pneumonia several months before this admission, and since required a four-times-daily care package.

During the current admission the patient had been treated for a further pneumonia on the basis of new chest x-ray changes, breathlessness and raised inflammatory markers. He had also undergone a CT chest/abdomen/pelvis for the unexplained weight loss. This was consistent with chronic COPD and bronchiectasis but no other positive findings. A week prior to ICU referral he was found to have acute kidney injury (creatinine 280 µmol/mL, baseline 90 µmol/mL) which had failed to improve. In the 24 hours prior to referral had become progressively drowsy and oliguric.

The patient appeared frail, cachectic and oedematous. He groaned in response to voice and could not follow commands. He had Kussmaul breathing at a rate of about 18 breaths per minute with SaO2 of 91% on 35% oxygen via facemask. Arterial blood gas showed pH 7.09, pCO2 7.1 kPa, pO2 9.1 kPa, base excess -9.3 mEq/L, lactate 1.3 mmol/L, glucose 8.7 mmol/L, creatinine 294 µmol/mL. His chest x-ray showed persistent bilateral patchy consolidation. He had a blood pressure of 98/55 mmHg with a pulse of 110 beats/min and cool peripheries. ECG showed sinus tachycardia. He was afebrile. Abdomen was soft and a urinary catheter had drained only 25 mL in the last 4 hours. Other than reduced responsiveness, neurological survey was non-diagnostic.

Evaluation of this patient revealed an elderly man who was severely unwell with acute kidney injury, probable sepsis, and a poor response to treatment to date. This was on the background of chronic suppurative lung disease, and diminished health for several weeks. No specific treatment limitations were in place. His next-of-kin was unaware of any prior expressed wishes and was under the impression that the patient would prefer active treatment. The referring team were of the opinion that intensive care should be considered.

Although no unifying diagnosis for this gentleman’s kidney injury had been identified, a single, rapidly-reversible condition was not apparent. The principal indication for intensive care was for renal replacement therapy for an unknown duration. In view of the status of his neurological, respiratory and cardiovascular systems, it was deemed that airway protection, invasive respiratory support and vasopressor treatment would almost certainly be required. His overall health status made the prospect of survival from a prolonged period of multi-organ support on intensive care highly unlikely. After discussion with the intensive care consultant and the referring consultant it was decided to withhold admission to the intensive care unit. Appropriate family discussions were held. The patient was actively managed on the ward for a further 12 hours, after which fluid management, antimicrobials and further investigation were ceased. He died the following day.

What uncertainties do we face when declining admission to intensive care?Read More »