ICU Fellowship Vivas – MH, Failure to Wean and Pancreatitis

Dr Swapnil Pawar July 28, 2021 912

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    ICU Fellowship Vivas – MH, Failure to Wean and Pancreatitis
    Dr Swapnil Pawar

Viva answers written by – Dr Madhuri Anupindi


  1. 75M admitted post MET call for tachycardia, 1 week after Whipple’s. Post-op course complicated by surgical site infection requiring IV antibiotics. He is receiving morphine and tramadol for analgesia, and regular haloperidol for delirium.

BG: diabetes, Graves’ disease and rheumatoid arthritis for which he takes regular prednisolone.

On ICU admission: confused, restless, diaphoretic with a temperature of 42 degrees. Provide a differential diagnosis for his fever and outline your management plan.

There are numerous potential infectious and non-infectious causes for this man’s fever.

Infectious causes:

  • Complications from original surgery:
    • Worsening of the wound infection
    • Anastomotic leak with intra-abdominal collections
  • Other hospital-acquired infections
    • Pneumonia
    • UTI
    • Line infection
    • C difficile
  • Less likely another pathology
    • Meningitis
    • Septic arthritis etc

Non-infectious causes:

  • Drug-related
    • Serotonin syndrome or neuroleptic malignant syndrome
    • Drug fever: antibiotics often implicated
    • Drug withdrawal (less likely)
    • Anticholinergic ?on other meds
  • Endocrine
    • Thyroid storm
    • Adrenal insufficiency
  • Inflammatory/autoimmune
    • Pancreatitis
    • Aspiration pneumonitis
    • Post transfusion
    • Seizures
  • Vascular
    • DVT/PE
    • CVA
    • Ischaemic bowel
    • Splenic or portal vein thrombosis

Management would involve simultaneous resuscitation including cooling, thorough evaluation and investigation of the cause of his deterioration, and specific and supportive management.


A – assess

B – sats and full monitoring, resp rate, supplemental oxygen, CXR

C – IV access, HR, BP, check lines, IVF bolus and assess fluid status, likely art line/CVC, vasopressors if required, culture widely

D – GCS, focal neurology and pupils,

E – BSL, start cooling, artic sun, blanket, cool fluids, ice packs, insert IDC with temperature sensor


Would involve history, exam and investigations

  • History
    • Infection: localising symptoms, signs, most recent imaging, recent culture results and sensitivities, duration of abx treatment
    • Non-infectious: medication review, allergies, recent transfusions, co-morbidities, steroid dose, drug/alcohol use, withdrawal signs
      • Medication review would include drugs that may inhibit the metabolism of some of the serotenergic drugs e.g. fluconazole inhibits CYP 219
    • Exam
      • Top to toe exam looking for signs of infection, abdominal exam, wound site
      • Check compartments
      • CNS exam: focal neurology, increased tone (serotonin syndrome, UMN lesion), pupils (dilated serotonin syndrome), clonus, reflexes, rigidity (lead pipe in NMS), tremor and lid lag (thyroid storm)
    • Investigations
      • Bedside: UA, ABG, ECG, CXR
      • Bloods: full-bloods FBC UEC LFT CMP coags CK, septic screen, TFTs, cortisol, glucose, troponin
      • Imaging: CTabdo +/- CTB

Specific management

  • Depends on cause
    • Infection à abx and source control
    • Non-infectious
      • Serotonin syndrome: Mx: cease offending drugs, sedation, cooling, cyproheptadine 12mg tds if drugs with long half-life (although use controversial)
      • NMS: Mx: cease offending drugs, bromocriptine (dopamine agonist) 2.5mg q8h, can use dantrolene, supportive care
      • Withdrawal: Benzos if alcohol withdrawal + thiamine and glucose
      • Drug fever: cease offending agents
      • Thyroid storm: Prevent thyroid hormone synthesis (propylthiouracil) or carbimazole, prevent release (inorganic iodine or lithium), prevent T4àT4 (propylthiouracil, propranolol, corticosteroids), prevent effects of thyroid hormone (propranolol, steroids), increased clearance (cholestyramine)
      • Adrenal insufficiency: Mx: hydrocortisone, treat the underlying cause
      • Pancreatitis: supportive

Supportive management

  • Analgesia
  • Nutrition
  • DVT prophylaxis
  • Notify family

How would you monitor the temperature in this patient?

I would do this via an IDC with a temperature sensor as it allows for the patient’s temperature to be measured continuously, he is very likely to require an IDC regardless, is considered to be reflective of core temperature and is recommended by current guidelines.

Briefly outline the potential methods of cooling this patient.

There are multiple non-invasive and invasive methods of cooling this patient.

Non-invasive methods include:

  • Passive cooling such as cooling the room and exposing the patient: this is often ineffective, slow and difficult to titrate the temperature
  • Active external cooling includes:
    • Use of ice packs or evaporative cooling with fans and wet skin: this is easy to implement and cheap but also slow and difficult to titrate the temperature. It may also cause issues with uneven cooling and with electrical safety.
    • Cooling vests or blankets: these often have feedback systems that can be coupled with temperature monitoring. They are often more effective at cooling but are also more expensive.

Invasive methods include:

  • Infusion of cold fluids: this is effective, easily available and cheap but can require significant volume of fluids to be infused which may cause electrolyte disturbances, arrhythmias, and fluid overload.
  • Intravascular cooling catheters: these are effective and can often be used as central lines but are expensive and not widely available
  • Body cavity lavage with cold fluids: can provide effective cooling but invasive and can cause electrolyte abnormalities
  • Extracorporeal cooling via ECMO or CRRT: provides very rapid cooling but is invasive and subjects the patient to the risks of vascular access and extracorporeal circuits

Many of these methods may not be tolerated by this patient in his current state due to his confusion, and may also cause shivering. Therefore, intubation may be required to facilitate temperature control and to reduce metabolic demand.

 What are the key features of malignant hyperthermia?
Malignant hyperthermia is a genetic disorder of skeletal muscle which allows for excessive myoplasmic calcium accumulation after exposure to certain agents resulting in sustained muscle contraction and breakdown. Common clinical features include:

  • Neurological: general muscle rigidity, masseter muscle rigidity, hypertonia
  • Cardiovascular: tachycardia and arrhythmias
  • Respiratory: hypercarbia, unexplained increase in etco2, tachypnoea
  • Metabolic: hyperthermia, sweating

Investigative features include:

  • ECG: arrhythmias and ECG changes of hyperkalaemia such as peaked t waves
  • Myoglobulinuria and raised CK
  • Mixed metabolic and respiratory acidosis
  • Hyperkalaemia
  • Organ dysfunction including acute kidney injury and DIC

What are the potential drugs used in ICU that can give rise to MH

The main potential drug which is used in ICU is suxamethonium. Volatile anaesthetic agents such as sevoflurane are also a common trigger, although these are rarely used within the ICU.


  1. 64 year old female, previously well, had right hemicolectomy complicated by an anastamotic breakdown with sepsis and multi-organ failure requiring a return to theatre. After 10 days in ICU, she remains oliguric receiving intermittent RRT but has otherwise had resolution of her organ failures. She was extubated this morning and required re-intubation 4 hours later. What are the possible reasons for her failed extubation?

Numerous potential causes, likely multi-factorial with a combination of complications from her prolonged stay in ICU and potentially new pathology


  • Delirium or agitation
  • Weakness: potential critical illness polyneuromyopathy given long stay in ICU with multi-organ failure à poor cough
  • Significant abdominal pain: difficultly taking deep breaths
  • Decreased elimination of sedatives causing drowsiness
  • New pathology such as stroke


  • New pathology such as ischaemia causing failure/pulmonary oedema
  • New shock
  • APO
  • Arrhythmia


  • Aspiration
  • Ileus causing increased abdominal distension


  • Fluid overload secondary to renal failure and exacerbated by loss of positive pressure
  • Metabolic acidosis causing tachypnoea


  • New infection
  • Significant sputum load
  • Post extubation stridor (less likely given 4 hours)
  • Atelectasis
  • Pulmonary embolism
  • Allergic reaction
  • Bronchospasm

How will you optimise her prior to her next extubation?

Optimisation would require identification and treatment of the contributors to her failed extubation. This would first involve a thorough evaluation including targeted history, exam and investigations.

History and exam particularly focused on:

  • Neurological: delirium, focal neurology, weakness including bulbar function and antigravity movement, adequacy of cough, medication review especially sedatives, steroids
  • Cardiovascular: haemodynamic status
  • Respiratory: sputum load, signs of infection, bronchospasm, support required from ventilator
  • Gastrointestinal: abdominal distension, bowels opened?
  • Renal: when last dialysed and fluid balance
  • Signs of sepsis, lines


  • Bedside: ABG looking at gas exchange and lactate, ECG for signs of ischaemia/arrhythmias, TTE for cardiac function if thought to be contributor
  • Bloods: organ function, septic screen if required, electrolytes
  • Imaging: CXR, consider CTB/chest/abdo depending on findings of investigation


  • Decrease respiratory resistance
    • Ensure ETT adequate size
    • Consider tracheostomy
    • Humidification, chest physio, bronchoscopy if significant sputum plugging with collapse
    • Bronchodilators if bronchospasm present
  • Improve respiratory compliance
    • Treat underlying lung disease/infection
    • Ensure ventilator settings appropriate
    • Decompress abdomen if contributing
  • Decrease respiratory work
    • Sit patient up
    • Decrease oxygen demand: treat fever/agitation, avoid overfeeding, adequate analgesia, correct acidosis
  • Increase oxygen supply
    • Treat myocardial dysfunction
    • Treat severe anaemia
    • Optimise fluid balance: aggressive fluid removal with dialysis as tolerated, may require low dose vasopressor support
  • Optimise ventilatory drive
    • Minimise sedation
    • Screen for and manage delirium
    • Avoid significant alkalosis
  • Optimise muscle function
    • Adequate nutrition
    • Intensive physiotherapy
    • Avoid steroids/neuromuscular blockers as able
    • Optimise electrolytes

What are the indications and complications of a tracheostomy?


  • To facilitate weaning from mechanical ventilation
  • To aid in sputum management
  • Upper airway obstruction
  • Airway protection from aspiration
  • Adjunct in significant head and neck surgery or trauma

Complications: these can be procedural, acute and chronic.


  • Airway fire
  • Bleeding
  • Injury to surrounding structures: false tract, surgical emphysema from pneumomediastinum or pneumothorax, trachea-oesophageal fistula, injury to posterior tracheal wall, recurrent laryngeal nerve injury, thyroid injury, tracheal ring fracture, cricoid fracture
  • Guidewire issues: loss, kink, fractured
  • Loss of airway
  • Loss of airway pressure
    • Hypoxia, derecruitment, pulmonary oedema, bradycardia, haemodynamic instability
  • Complications of foreign material in airway: bronchospasm, aspiration pneumonitis
  • Malpositioned or incorrect size


  • Tube displacement
  • Infection
  • dysphagia
  • Post obstructive oedema
  • Mucus plugging
  • Bleeding


  • Tracheal stenosis
  • Tracheoesophageal or tracheocutaneous fistula
  • Tracheomalacia
  • Tracheitis
  • Bleeding, tracheo-inominate fistula
  • Voice change and chronic cough
  • Pneumonia
  • Swallowing difficulties
  • Sternoclavicular osteomyelitis
  • Scarring and cosmetic issues

What is the optimal timing of a tracheostomy and is there evidence for same?

There is no consensus on the optimal time to perform a tracheostomy as this is dependent on the individual patient and environment. An ‘early tracheostomy’ is generally thought of as those performed within 10 days of intubation. Proponents hypothesise that early tracheostomy may allow for less sedation, improved patient comfort, fewer complications from an oral endotracheal tube, shorter ICU stay and therefore reduced morbidity and mortality. Proponents against state that it subjects more patients to the risks of tracheostomy, some of whom may not go on to actually require thm.

The major trial regarding timing was TracMan from 2013 which studied 909 intubated patients who were thought to require at least 7 more days of ventilatory support. They were randomised to undergo a tracheostomy within 4 days of ICU admission or after day 10. There was no mortality difference between the two and no statistically significant difference in duration of mechanical ventilation or ICU length of stay. However, this trial did not include patients who may have required a tracheostomy for non-respiratory reasons and less than half of the patients in the ‘late’ group ended up requiring a tracheostomy.

A Cochrane review in 2015 of almost 2000 patients (the majority of which come from TracMan) found a statistically significant mortality benefit from early tracheostomy with a number needed to treat of 11, and that the early group and a decreased duration of sedation but no significant decrease in duration of mechanical ventilation. However, they advised that these findings were only suggestive as there was minimal high quality evidence available.

The optimal timing of tracheostomy is ambiguous and not well established. Some patients such as those with significant neurological dysfunction or severe facial burns may benefit from early tracheostomy. Decisions regarding timing relies on clinical experience and consideration of individual patient factors.

  1. 56M with 2 day history of severe epigastric pain and vomiting in the ED. Conscious, distressed, BP 75/45mmHg, HR 120, RR 38, temp 38.6, sats 91% RA. Abdomen is distended and diffusely tender without guarding. He is oliguric. What are your differential diagnoses and how would you investigate this patient?

This patient is shocked and requires urgent simultaneous resuscitation, evaluation and treatment. I am concerned that he has severe pancreatitis but other possible differentials include:

  • Hypovolemic shock: aortic dissection, leaking AAA
  • Cardiogenic shock: ischaemia
  • Distributive shock:
    • Sepsis: intra-abdominal pathology: biliary sepsis, colitis,
      • Non-intra-abdominal: severe pneumonia
    • Vascular: mesenteric ischaemia, ischaemic bowel
    • Adrenal crisis
    • Trauma: Boerhaave’s syndrome, perforated viscus


  • Thorough history
    • Presenting complaint
      • Pain: radiation, exacerbating/relieving factors, similar episodes, quality, associated symptoms (neuro symptoms/signs dissection, infective symptoms, SOB/diaphoresis)
      • Vomiting: characteristics, bowels ?open
    • Co-morbidities/meds/allergies
      • AF (mesenteric ischaemia), IHD, peripheral vascular disease, peptic ulcer disease, recent trauma, steroid use
      • Risk factors for pancreatitis: alcohol use, triglycerides, HIV, gallstones, drugs (furosemide, thiazides, steroids), ERCP, SLE
    • Exam
      • Vitals, HR and rhythm
      • Neuro signs – dissection
      • Radial-radial delay for dissection
      • Auscultation of chest: bronchial breath sounds, murmurs
      • Auscultation of bowel: tinkling bowel sounds in SBO
      • Palpable AAA
    • Investigations
      • Bedside: ECG (ischaemia, AF), ABG (lactate, BSL, electrolytes, metabolic parameters), CXR erect (free air, pneumonia, widened mediastinum, pneumomediastinum), UA (UTI/pyelo) and culture – insert IDC for urine output
      • Bloods: lipase (pancreatitis), blood cultures, FBC (anaemia, leucocytosis), UEC (renal function), CMP, LFT (hepatitis and for Ranson score), LDH, coags (DIC), consider cortisol if concerns re adrenal crisis, G+H, consider troponin, triglycerides for cause
      • Imaging: likely CT abdomen, if pancreatitis then US abdomen to look for gallstones ?cause

On investigation, his lipase is 2000 and CT abdomen confirms a diagnosis of pancreatitis. How will you manage him?

 Management consists of resuscitation, logistic, specific and supportive management.


  • A + B: supplemental oxygen, full monitoring
  • C: large-bore IV access, fluid resuscitation, likely arterial line and CVC – vasopressor support
  • D: analgesia
  • E: antipyretics, insert IDC to monitor fluid balance and urine output


  • Admit to ICU
  • Surgical involvement

Specific management

  • Evaluate for local complications: look at CT for signs of local complications such as necrosis, abscess or collections
    • Repeat CT during the stay as a progress scan or earlier if patient’s condition deteriorates
    • Collections may need percutaneous or endoscopic drainage
    • High suspicion for abdominal compartment syndrome
  • Optimise organ support and minimise systemic complications
    • Judicious fluid management with vasopressor support
    • Respiratory optimisation with adequate analgesia, decompression of abdomen with NGT, chest physio and supplemental oxygen
  • Treatment of cause
    • Insulin infusion if hypertriglyceridemia
    • ERCP if biliary pancreatitis with concurrent cholangitis

Supportive management

  • DVT prophylaxis
  • Nutritional support
  • BSL control aiming 6 – 10.

He continues to be febrile, your registrar asks about commencing antibiotics, what will you tell her?

There is no role for routine prophylactic antibiotics in pancreatitis and no evidence that it improves patient-centred outcomes. I would consider commencing antibiotics if:

  • The patient remained severely shocked despite fluid resuscitation and was requiring high dose vasopressor support
  • He developed necrotising pancreatitis with positive cultures or a pancreatic abscess
  • There was high suspicion of an extrapancreatic infection

How will you approach his nutrition?

Enteral nutrition is preferable to parenteral nutrition. Assuming this patient has severe pancreatitis, I would start enteral nutrition within 48 hours via an NG or NJ tube at a low rate and slowly increase as tolerated aiming 25 – 35kcal/kg/day. I would only start TPN if enteral nutrition is not tolerated after 5- 7 days.


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