Category: Year

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

Echocardiography on ICU

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A 50 year old female presented with acute kidney injury and sepsis.  She required fluid resuscitation, haemofiltration and cardiovascular support for 2 days, following which she was discharged to the renal ward for on-going haemodialysis. She underwent dialysis every 2-3 days for the next 3 weeks. Whilst on the ward she deteriorated acutely one evening, developing respiratory distress, followed by a respiratory arrest. She was intubated and ventilated transferred to the critical care unit.

A CTPA was negative for pulmonary embolus, but showed large bilateral pleural effusions. Tracheal suctioning was initially clear but later copious blood stained secretions were removed. A bedside cardiac echo performed by the consultant intensivist showed a globally sluggish left ventricle, which was overfilled, and the inferior vena cava measured 3cm also suggesting fluid overload. A trial of furosemide failed and she was aggressively haemofiltered to remove the excess fluid. Troponin was only mildly raised, and not thought to be suggestive of an acute cardiac event. She was extubated 24 hours later, but had two further episodes of flash pulmonary oedema requiring non-invasive ventilatory support whilst haemofiltration was re-commenced for fluid balance reasons. In total twelve litres of fluid were removed, with significant improvement in the patient’s condition. Repeat echocardiography prior to discharge showed an improving left ventricular function and IVC measurement of 2cm with greatly increased compliance.

What is the evidence that focussed echocardiography helps guide decision-making in intensive care?Read More »

Albumin Use in Critical Illness

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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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Predicting Weaning from Mechanical Ventilation

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A 60 year old man was electively admitted to the intensive care unit following a combined kidney pancreas transplant. Diabetes mellitus was the cause for his end stage renal failure. He was admitted for overnight HDU care, and was discharged the following day. He had delayed graft function thought to be related to a prolonged cold ischaemic time of the kidney. He would need dialysis until the function of the transplanted kidney improved. Four days later whilst on the ward he became hypotensive, became unconscious and suffered a cardiac arrest. He was successfully resuscitated and was readmitted to ICU.

In the ICU he required a blood transfusion as his haemoglobin level had dropped. He was taken to theatre for a re-laparotomy and a graft pancreatectomy was performed and all bleeding was stopped.

He continued to suffer from delayed kidney graft function and needed intermittent dialysis. After two days he was on minimal respiratory support and on sedation hold was deemed ready for extubation. He was extubated successfully and remained so for the next 12 hours. He then had an episode of bradycardia and had a markedly reduced cardiac output. He was re-intubated and stabilised. A temporary pacing wire was inserted to control potential episodes of bradycardia.

His condition remained stable over the next day and was again extubated. His oxygenation needs increased over the next 12 hours and was placed on non- invasive ventilation. This stabilised him over the next 12 hours but he suffered from retained secretions and was re-intubated. He then suffered with an ileus and had abdominal distension which complicated his respiratory function. He had a tracheostomy placed and remained on mechanical ventilation for 2 weeks. He was difficult to wean as he suffered set backs related to acute sputum retention and a ventilator associated pneumonia.

This patient had been extubated twice with some degree of morbidity associated with it as he had to be reintubated. It would also be reasonable to assume that this increased his length of stay on the ICU slowed down his ICU discharge. Deciding when to extubate a patient seems to be still a difficult decision to make in some cases and the experience of senior clinicians remains an important role.

For those who have not accumulated this level of clinical experience are there tools available to help them in deciding when and who could be weaned and extubated from mechanical ventilation?Read More »

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 »

Acute Mitral Valve Failure

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An elderly woman woke from sleep with acute breathlessness and wheeze. She had been treated for late-onset asthma by her GP. She had no other previous medical history and was exceptionally active. In the emergency department she received standard treatment for acute severe asthma . A systolic murmur was noted and an echocardiogram requested. After 24 hours of relative stability she experienced a sudden deterioration in her breathing and despite increased therapy for her asthma she had a respiratory arrest.

Following resuscitation and emergency tracheal intubation she was transferred to the ICU. On examination she was peripherally cool. Chest auscultation revealed extensive wheeze and crackles. Investigations revealed a raised troponin I (0.92 ug/L) and raised BNP (530 pmol/L). Her CXR revealed pulmonary oedema and her ECG showed sinus rhythm without overt evidence of ischaemia.

Initial problems included poor oxygenation, oliguria and a low cardiac output state (LiDCO revealed cardiac index of 2.1 l/min/m2). She received norepinephrine (up to 0.6 mcg/kg/min) and dobutamine (up to 40 mcg/kg/min). Levosimendan was introduced to augment her cardiac function as her CI had not achieved to 2.5l/min/m2. Norepinephrine was increased to maintain a MAP over 65mmHg. After levosimendan her urine output, acid-base status and CI were not substantially improved. The dobutamine had been stopped and she remained on norepinephrine.

An echocardiogram revealed hyperdynamic LV and RV and mitral regurgitation, which was initially assessed as being moderate in severity. Cardiac surgical opinion was that the risk of mitral valve surgery was unacceptably high.

Over the following few days she had problems with recurrent compromising atrial fibrillation and was treated with varying degrees of success with a variety of measures including DC cardioversion, amiodarone, metoprolol, digoxin and verapamil. Diuresis was obtained with a frusemide infusion and ramipril was introduced. Her CXR appearances improved and ventilation became easier.

On the 3rd day a trans-oesphageal echocardiogram confirmed severe mitral regurgitation (MR) with prolapse of the posterior mitral valve (MV) leaflet due to a ruptured chordae tendinae. There was resultant left atrial enlargement and pulmonary hypertension with an estimated PA systolic pressure of 60-70mmHg. Within a week she was weaned from ventilatory support and recovered sufficiently to mobilise independently prior to discharge home.Read More »

Arthrogryposis & Paediatric Difficult Airway

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EMERGENCY MANAGMENT OF A DIFFICULT AIRWAY IN AN INFANT WITH ARTHROGRYPOSIS MULTIPLEX CONGENITA

A 4 month old infant with arthropgryposis multiplex congenital was admitted to the paediatric assessment unit. The infant had been acutely unwell over the preceding 12 hours with respiratory compromise and a productive cough with green sputum. He had signs of respiratory distress with a RR of 40, pulse oximetry showed SpO2 of 85% on air and only 90% with a facemask, reservoir bag and high flow oxygen. It was felt that the infant would need to be intubated and ventilated. Two months before the infant had had a respiratory arrest on the neonatal ward and was unable to be intubated. That situation was resolved by mask ventilation and rescue with an LMA. There were obvious concerns that direct laryngoscopy would be unsuccessful and may precipitate a terminal decline in the patient’s condition.

The infant’s breathing was supported by bag/mask ventilation whilst he was transferred to an ENT theatre. Further anaesthetic support and an ENT surgeon were sought. I.v. access was established through a scalp vein. Ventilation was switched to an Ayres T piece with Jackson-Rees modification. Induction of anaesthesia was initiated with sevoflurane and oxygen. Direct laryngoscopy showed a Lehane and Cormack grade 4 view.

A rigid bronchoscope with video camera monitor was used by the ENT surgeon to obtain a view of the glottis. An epidural catheter was placed down the side port of the bronchoscope and was directed through the vocal cords. The bronchoscope was removed and a fine bore suction catheter was railroaded over the epidural catheter to give more stiffness. The positions of the end of the catheters were checked with the bronchoscope. A size 3.0cm uncuffed endotracheal tube was then railroaded over the catheters into trachea. Position and length were confirmed with the bronchoscope and ventilation was continued. The arrangement is shown in Figure 1.

The child was then transferred to the adult ICU where a retrieval team arrived to transfer the patient to a PICU.

What is arthrogryposis? Describe some methods for achieving control of the difficult paediatric airway.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 »