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ICU Fellowship Vivas – TTM, Wernicke’s encephalopathy, and Post AAA repair management

Dr Swapnil Pawar April 20, 2022 298 1

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    ICU Fellowship Vivas – TTM, Wernicke’s encephalopathy, and Post AAA repair management
    Dr Swapnil Pawar


Written by – Dr Madhuri Anupindi

  1. 65M OOHCA receiving 6microg/min of adrenaline with a BP of 100/70mmHg, anuric for the last 2 hours, GCS of 6, temperature is 37.6 degrees. What factors would you take into consideration in managing this patient’s temperature?

This would involve consideration of patient and logistic factors.

Patient factors

  • Suitability for targeted temperature management
    • Neurological status: currently GCS 6 so would be suitable
      • If conscious and able to follow commands then may not require as intensive temperature management
    • Arrest circumstances: may not be major consideration
      • Uncontrolled bleeding
      • Traumatic arrest
    • Patient’s current state
      • Haemodynamic status
    • Co-morbidities and ongoing treatment aims
  • Potential adverse effects of cooling
    • Haemodynamic instability: arrhythmias, hypotension, bradycardia
    • Mild coagulopathy
    • May have risk of infection
    • Shivering
    • Decreased gut motility
    • Decreased tubular resorption in kidney  diuresis/electrolyte derangement

Logistic factors

  • Institutional
    • Practice
    • Staffing
  • Temperature control related
    • Devices available to measure and control temperature

What temperature would you aim for and how would you achieve this?

I would aim for normothermia – maintaining a temperature < 37.8.

I would measure core temperature using a bladder temperature probe and ideally have this coupled with a feedback-controlled surface cooling system such as a blanket or vest if available.

What is the rationale behind temperature management?

The exact mechanisms by which targeted temperature management may be beneficial have not been fully elucidated. The potential reasons include:

  • Avoiding fever: this may decrease metabolic demand and neuronal injury
  • Decreased ischaemic-reperfusion injury
    • Decreased ion pump dysfunction, influx of calcium into cells and neuroexcitotoxicity
    • Decreased cell membrane leakage, cytotoxic oedema
    • Decreased production of free radicals
    • Decreased production of toxic metabolites
    • Decreased metabolic demand and oxygen consumption
    • Decreased release of excitatory neurotransmitters such as glutamate and aspartate
    • Decreased inflammatory response
  • Decreased cerebral oedema
    • Decreased permeability of blood brain barrier
    • Decreased vascular permeability
  • Intrinsic anticonvulsant effect

What is the evidence for targeted temperature management post out of hospital cardiac arrest?

The most recent evidence from TTM2 suggests that targeting hypothermia does not result in improved outcomes compared to targeting normothermia after out of hospital cardiac arrest.

TTM2: NEJM 2021

  • Multicentre, international, randomised control trial of 1900 adults with out of hospital cardiac arrest of presumed cardiac or unknown cause who had sustained return of spontaneous circulation and remained unconscious (FOUR score motor response < 4 and not able to obey verbal commands)
  • Intervention was targeted temperature of 33 degrees for 28 hours followed by controlled rewarming
  • This was compared to a targeted normothermia group who had a target temperature of 37.5 degrees with early treatment of fever if temperature was ³8
  • There was no difference in all cause mortality at 6 months or secondary outcomes including functional outcome,, health related quality of life or adverse events except for a higher rate of arrhythmias with haemodynamic instability in the hypothermia group

This study supports findings from the previous TTM trial in 2013 which showed that there was no difference in mortality or neurological outcomes for patients treated with hypothermia to 33 degrees compared to 36 degrees after out of hospital cardiac arrest of presumed cardiac cause.

  1. 34F who has presented with malaise and confusion. BG: previous morbid obesity and underwent bariatric surgery in the last 6 months with extensive weight loss. She has been intubated for lowered conscious state in the ED. Exam: dehydrated, afebrile, BP 120/80, HR 118, sats 99% on fio2 of 0.4. Prior to intubation she was noted to have bilateral nystagmus. What is the differential diagnosis?

Multiple potential causes but my primary differential is Wernicke’s encephalopathy given the history of weight loss, altered level of consciousness and nystagmus. Other potential causes include:


  • Vertebrobasilar ischaemia
  • Cerebellar haemorrhage

Malignancies including tumour affecting third ventricle, lymphoma, metastatic cancer


  • CNS infection including herpes encephalitis or HIV encephalitis
  • Cerebellar abscess
  • Viral cerebellitis: CMV, EBV, West Nile
  • TB
  • Progressive multifocal leukoencephalopathy
  • Malaria
  • Fungal meningoencephalitis

Drug induced

  • Alcohol
  • Phenytoin
  • Barbituates
  • Lithium
  • Benzodiazepines
  • Amitryptylline withdrawal
  • Polypharmacy overdose


  • Hepatic encephalopathy
  • Electrolyte disturbances: Mg, sodium, calcium, PO4
  • Endocrine disturbances: hypothyroidism (although unlikely with tachycardia), hypoparathyroidism
  • Hypoglycaemia
  • Vitamin B12 deficiency, vitamin E deficiency, Zinc deficiency

Autoimmune, idiopathic

  • Cerebral vasculitis
  • Multiple sclerosis
  • Seizures  multiple causes
  • Normal pressure hydrocephalus
  • Acute disseminated encephalomyelitis
  • Neurosarcoidosis

How would you further assess this patient?

The assessment would involve history, exams, and investigations.

History: Collateral history including

  • Timing/onset of confusion and malaise
  • Weight loss/diet
  • Associated symptoms including infective symptoms, other neurological symptoms
  • Co-morbidities
  • Medications
  • Drugs/alcohol


  • Vitals including temperature
  • Full neurological exam including cranial nerves (as able while intubated)
  • Signs of nutritional deficiencies (macro/micro)
  • Signs of infection including CNS: meningism
  • Signs of organ impairment: liver, renal, cardiac, resp


  • Bedside
    • ECG
    • ABG
    • UA
    • TTE: may have signs of heart failure, can have dilated cardiomyopathy
  • Bloods
    • Organ function/electrolytes
    • Red cell transketolase (but often takes days to come back)
    • Blood cultures
    • BHCG
  • Imaging
    • CXR: Intubated/line tubes
    • CTB
    • Consider MRIB
  • Other (depending on history)
    • LP
    • EEG

What are your management priorities?

  • Identify the cause and complications of deterioration
    • Specific treatment will depend on the same
  • Supportive treatment
    • ICU admission, full monitoring and access
    • Lung protective ventilation
    • Neuroprotective care
    • Nutritional optimisation
      • NG feeds – monitor for refeeding
      • Dietician review
      • BSL control
    • DVT prophylaxis
    • Support of family

What is the pathogenesis of Wernicke’s?


  • Thiamine is a cofactor for key enzymes important in energy metabolism including transketolase and pyruvate dehydrogenasea
  • Thiamine requirements depend on metabolic rate  increased demand during high metabolic demand and high glucose intake
  • Deficiency in thiamine means that metabolically active tissue is unable to synthesise ATP
  • Thiamine required for cerebral energy utilisation  deficiency causes neuronal injury by inhibiting metabolism, may cause BBB breakdown, NMDA excitotoxicity, increased ROS
    • Limited storage in body: 30mg, stores last about 1 month

What are the risk factors and clinical features of Wernicke’s?

Risk factors:

  • Decreased intake
    • Anorexia, alcohol, malnutrition, hyperemesis gravidarum, liver disease
  • Decreased absorption
    • GI disease: inflammatory or surgery
    • alcoholism
  • Increased depletion
    • Diuretics
    • Diarrhoea
    • Dialysis
    • Liver disease
  • Catabolic states
    • Sepsis
    • Hyperthyroidism
    • Pregnancy
    • Metastatic malignancy

Clinical features:

  • Classic triad
    • Encephalopathy: disorientation, inattentiveness, impaired memory, lethargy
    • Oculomotor dysfunction: nystagmus most common finding – usually horizontal, lateral rectus palsy bilateral, conjugate gaze palsies, anisocoria
    • Gait ataxia: broad based gait
  • Other: hypotension, hypothermia, peripheral neuropathy, raised lactate, Beri Beri, delirium, vestibular dysfunction without hearing loss, tachycardia, exertional dyspnoea, elevated cardiac output

Briefly outline the diagnosis and treatment?


  • 2 of the 4 Caine criteria: dietary deficiency, oculomotor abnormalities, cerebellar dysfunction, altered mental status or mild memory impairment
  • Red cell transketolase measurement (but blood level may not reflect brain thiamine level)
  • Exclude other causes: organ function, septic screen, imaging


  • IV thiamine 300 -500mg tds for 3 days then decrease + glucose (thiamine cofactor for Krebs cycle)
  • Replace magnesium (co-factor for thiamine deficiency), potassium and phosphate
  1. 64M who had an emergency AAA repair last night. His sedation has been ceased in anticipation of extubation, but nurses are concerned that he appears to be in a lot of pain. BG: IHD, T2DM, chronic back pain for which he has been on long term opioid treatment. Outline how you would assess this situation?

My concerns are that his pain is either due to a complication of the AAA, a new event or acute pain secondary to the surgery on a background of chronic back pain. My assessment would involve a targeted history, examination and investigations.


  • Co-morbidities/medications/allergies
    • Chronic back pain: amount of opioids he was on, level of function, neuropathic element
    • IHD: previous surgery/PCI, TTE, ECG
    • T2DM: renal involvement (NSAIDs likely contraindicated, may not benefit from high dose morphine), diabetic
  • AAA:
    • Surgical/anaesthetic details, any complications, blocks/local anaesthetic infiltration
    • Trajectory in ICU: amount of analgesia


  • Vitals and stability: exclude acute complications
  • Neurological function: able to point where pain is (abdominal, chest, back)
  • Chest: new signs of failure, murmurs
  • Abdominal exam: leak, acute abdomen, ACS


  • Exclude acute pathology:
    • Bedside: ECG (ischaemic changes), ABG (lactate, metabolic parameters), TTE (wall motion abnormalities)
    • Bloods: FBC, coags, organ function, consider G+H, ROTEM, troponin
    • Imaging: potentially CTA abdomen

How would you manage?

Exclude complications of surgery/new pathology

  • Treatment will depend on the findings of the assessment

Supportive Management

  • Multimodal analgesia
    • Regular paracetamol
    • Calculate normal dose of opiates and give same + extra
    • Neuropathic agents
    • Unlikely NSAIDs will be suitable
  • Ensure pain well controlled prior to extubation


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