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ICU Fellowship Vivas – Morbid Obesity, Digoxin Toxicity & Traumatic hepatic injury

Dr Swapnil Pawar November 22, 2021 430

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    ICU Fellowship Vivas – Morbid Obesity, Digoxin Toxicity & Traumatic hepatic injury
    Dr Swapnil Pawar

Podcast Script Written by Dr Madhuri Anupindi

1. You have been called to assist at the resuscitation of a 27 year old patient in cardiac arrest on the general ward of your hospital. The patient is on the floor, with the surgical JMO attempting ventilation with a bag and mask, and a nurse performing chest compressions. The patient has super morbid obesity with a BMI > 60kg/m2. What is your approach and what are the issues that you would consider in performing resuscitation in these circumstances?

This is a difficult situation due to the patient’s body habitus, his location on the floor and staffing. My approach would be to confirm the arrest, use the ALS algorithm, with certain modifications given the logistics involved.

Routine ALS algorithm would involve:

  • Calling for extra help: given this gentleman’s size will have significant issues with airway management, CPR, IV access and positioning
  • Allocating roles: airway (most experienced operator), CPR – two or three people to switch every 2 minutes and ensuring effective CPR, defibrillator/drugs, IV access, scribe, team leader
  • Attach defibrillator and evaluate whether shockable or non-shockable and continue as per algorithm
  • IV access if not already present may need US guided or IO or early central access although all difficult with obesity, can give adrenaline through ETT
    • Drugs that can be given via ETT include adrenaline, lignocaine and atropine
    • Administer 3 – 10 times the IV dose diluted in 10ml of sterile water, follow the dose by a minimum of 2 vigorous ventilations
  • Evaluating for reversible pathology: (history, exam and investigations) gaining further history, exam findings ? swollen leg, recent medications, OSA, recent ECG/chest pain, electrolytes, blood

Issues specific to this circumstance are patient-related and staff/environment-related.

Patient-related mainly stem from his super morbid obesity and relate to both assessment and management

  • Airway:
    • Likely to be difficult BVM and intubation in terms of position, especially since on floor requires senior operator, airway adjuncts, video laryngoscope, D blade, etco2 on BVM to see if able to adequately oxygenate/ventilate
    • Consider ramping to improve position if intubating
    • LMA may not be able to adequately oxygenate/ventilate
    • Difficult surgical airway
    • Increased risk of aspiration
    • Assess for signs of ?fall/trauma potentially requires C spine precautions but airway takes priority
  • B:
    • Decreased functional residual capacity and increased co2 production and ventilatory needs.
    • More difficult to ventilate with higher airway pressures
    • Difficult to auscultate for breath sounds and to perform procedures such as chest drains or needle decompression if required
  • C:
    • Impaired LV contractility, hypertension, peripheral vascular disease and coronary artery disease are more common.
    • Difficulty with clinical assessment: palpating pulses, obtaining BP – cuff size may be too small, assessing fluid status
    • Difficult with IV access – increased risk of complications, IO access may be impossible
    • Difficulty obtaining arterial access
    • Difficult to perform pericardial drains
    • May be difficult to perform effective CPR considering mechanical CPR device
  • Investigations will be difficult to perform such as XR, CT scan, blood tests, TTE
  • Potentially reversible causes difficult to identify and also to provide treatment
    • Hypoxia –  obesity increased risk VTE, impaired LV/RV, pulmonary hypertension, OSA, obesity hypoventilation, Co2 retention, ischaemic heart disease
    • Toxins: optimal dosing for many drugs in obesity is unknown
    • VTE: difficult to assess and ?what is adequate dosing of anticoagulation
    • Potentially tamponade or tension pneumothorax but difficult to diagnose and treat
    • Hypovolemia difficult to clinically assess
    • Hyperkalaemia ?CK with rhabdomyolysis


  • Junior staff: requires more assistance
  • Patient on floor: going to be very difficult to get him back into bed especially with resuscitation see if hover hoist available and likely transit time but likely to be safer to resuscitate on the floor
  • Staff occupational and safety issues – increased risk of injury to staff with manual handling

2. A 56M is brought to ED with trauma following an MVA. His initial blood tests reveal the following: raised AST (730), ALT (1034), mildly raised ALP (130), GGT (94) with normal bilirubin, albumin and INR. BSL 12.1. What is your interpretation of these results?

This  shows a transaminitis with minimal obstructive features and no evidence of synthetic dysfunction. This is most likely secondary to a traumatic hepatic injury but other potential causes include:

  • Acute derangements secondary to ischaemic hepatitis, right heart dysfunction or toxins consumed prior to the MVA e.g. alcoholic hepatitis, paracetamol overdose
  • Chronic: viral hepatitis, malignancy, fatty liver, metabolic derangements e.g. haemochromatosis, Wilson’s disease

How is hepatic trauma diagnosed?

The liver is one of the most commonly injured solid organs in blunt and penetrating abdominal trauma. Injuries to the chest wall are also often associated with significant liver injury.

Clinically patients may have right upper quadrant or shoulder tip pain, generalised abdominal pain or chest wall tenderness. There may be haemodynamic instability or peritonism depending on the extent of the injury. Signs of injury to the lower chest or thoracoabdominal region raises the index of suspicion of a hepatic injury.

Blood tests may show abnormal liver function tests, especially elevation of the AST and ALT. A FAST scan may show free fluid in Morrison’s pouch, the hypoechoic rim of subcapsular fluid or intraperitoneal fluid around the liver. The definitive investigation is a CT scan with contrast which can define the grade of liver injury and identify other injuries. In cases where the patient is too unstable for CT scan, the liver injury may be diagnosed during exploratory laparotomy.

How are liver injuries graded?

The degree of liver injury is graded from 1 – 5 using the American Association for the Surgery of Trauma (AAST) Hepatic Injury Scale. The grade is based on the highest grade assessment made on imaging, at operation, or on the pathological specimens. The grades depend on the size of the haematoma, the depth of any laceration, vascular injury and the extent of parenchymal disruption.

What are the basic principles of management of traumatic liver injury?

Initial stabilisation and resuscitation using ATLS approach of primary and secondary survey to identify and manage life threatening injuries

  • Includes adequate monitoring and IV access
  • Investigations including blood tests such as group and hold, imaging
  • May include supportive treatment such as ADT, IV fluids, transfusion of blood products aiming for haemostatic resuscitation

Definitive management of the liver injury depends on haemodynamic stability and grade of the injury:

  • If haemodynamically unstable or other indications for surgery exploratory laparotomy aiming to identify and control haemorrhage
    • This may initially be a damage control approach with the packing of the liver if the patient is very unstable
  • Haemodynamically stable and no indication for exploration
    • Close observation can often discharge if normal abdominal exam, stable haemoglobin for at least 24 hours and no other injuries requiring a hospital stay
    • Grade 1 -2 often conservative
    • Grade 3 -4: more likely to fail conservative management requiring surgery or angioembolisation, low threshold for ICU admission for higher-grade injuries
      • Embolization considered if there is evidence of ongoing bleeding and a contrast blush seen on CT
    • Generally, there is a lower threshold for the operative management in penetrating injuries such as stab wounds where exploration of the wound is often required

Monitor and treat complications including

  • Delayed haemorrhage
  • Hepatic abscess
  • Hepatic necrosis
  • Hepatic pseudoaneurysm
  • Biliary complications such as
    • Bile leak, biloma, bile peritonitis
    • Arterio-biliary or Porto-biliary fistula causing haemobilia

3. A 73F admitted following a collapse. She has a history of 3 days of anorexia, nausea, diarrhoea, vomiting and palpitations. BG: heart failure, T2DM, AF, HTN, COPD. Meds: furosemide, digoxin, amiodarone, metformin, aspirin, omeprazole, atorvastatin and salbutamol inhaler. Her initial observations are HR 51, BP 100/65, RR 30/min, sats 93% RA. Blood results show Hb 110g/L, WCC 14.9, platelets 148, K 6.5, urea 29.5, creatinine 223, glucose 3.5, lactate 7.1. Outline your differential diagnosis.

This lady has evidence of shock with end-organ impairment. I am concerned about digoxin toxicity given her bradycardia, vomiting and acute kidney injury, but this may be the primary cause of her presentation or secondary to another underlying pathology including:

  • Infection
    • Septic shock with multi-organ impairment multiple potential sources
    • Gastroenteritis causing hypovolemia and accumulation of digoxin/metformin
  • Cardiac
    • Exacerbation of cardiac failure
    • Myocardial ischaemia
    • Complete heart block or other arrhythmias
  • Respiratory
    • PE with right heart failure
  • Vascular
    • UGI bleed
    • Ischaemic bowel
  • Neurological
    • Subarachnoid haemorrhage
  • Drugs
    • Digoxin toxicity
    • Metformin toxicity

Briefly outline the other investigations you would order to help aid management

Investigations: tailoring the investigations would depend on findings of history/exam

  • Bedside: ECG for heart block/ arrhythmias, UA and MCS for infection, TTE to evaluate cardiac function, ABG
  • Blood: cultures, LFTs, coags, fibrinogen, digoxin level, troponin
  • Imaging: CXR, further imaging such as CTB/Abdo depending on exam findings

What ECG findings are observed with acute digoxin toxicity?

Digoxin causes increased automaticity as well as an AV conduction block so can cause multiple ECG findings include:

  • Tachyarrhythmias
    • Bidirectional ventricular tachycardia: very rare
    • Accelerated junctional rhythms
    • Multiple PVCs
    • VT or VF
  • Bradyarrhythmias:
    • AV blockade
    • SA node arrest
    • AF with complete heart block and junctional or ventricular escape rhythm

It is important to note that digoxin effect: ST depression in a concave shape or ‘reverse tick’ pattern, biphasic, inverted or flattened T waves, shortened QT interval, prolonged PR interval on ECG is DIFFERENT to digoxin toxicity.

What factors increase the risk of digoxin toxicity?


  • Enhanced absorption
    • Macrolides
    • PPIs
  • P glycoprotein inhibitors
    • Calcium channel blockers: verapamil and diltiazem
    • Amiodarone
    • Spironolactone
    • Quinidine

Electrolyte imbalance

  • Hypokalaemia
  • Hypomagnesemia
  • Hypercalcemia


Decreased elimination:

  • Renal disease
  • Dehydration

Increased age

What antidote is available for acute digoxin toxicity and what are the indications for its use?

Digoxin immune antigen-binding fragments (Digibind or Digifab) is a monovalent immunoglobulin that has a much greater affinity for digoxin than the Na/K/ATPase digoxin receptor sites. By binding to digoxin it prevents digoxin from binding to its receptor and creates a concentration gradient from the intracellular to the extracellular space, allowing for more digoxin to be extracted from the intracellular space. The Digoxin bound to DigiFab is then renally excreted. Total digoxin levels will remain high with DigiFab as the level measures both the bound and free Digoxin. Consequently, measuring Digoxin level post-administration has no correlation with ongoing toxicity. One vial of DigiFab will bind about 0.5mg of digoxin. The dose given depends on whether the toxicity is thought to be acute or chronic, whether the dose of ingestion is known, the serum digoxin concentration and the weight of the patient.

The indications for its use (as per TGA) are the treatment of known or strongly suspected life-threatening digoxin toxicity associated with ventricular arrhythmias, progressive bradycardia or second or third-degree heart block unresponsive to atropine, and where measures other than withdrawal or Digoxin and correction of electrolytes are thought to be necessary.

However, DigiFab has minimal side effects and no absolute contraindications except for hypersensitivity to any of the substances, so these indications are flexible.

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