March 11, 2010

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Laboratory Tester #003

March 11, 2010 By Chris Nickson 2 Comments

A 10 year-old boy with a history of enuresis was BIBA to the ED after a first episode generalized tonic-clonic convulsion. He seemed tired in the morning but still attended his inter-school sports competition. While getting ready to compete he collapsed and had a self-limiting seizure (5 minutes duration).

He was afebrile and had GCS 13 (E3 V4 M6) (fluctuating) for about 4 hours without improvement. Pupils were equal and reactive and he had no focal neurological deficits. He vomited 5 times during this time but was clinically euvolemic. His CT head was normal. After returning from the scan he had another self-limiting seizure that lasted 2 minutes.

He had the following laboratory test results (between seizures):

UEC

Na 123 mmol/L    (134-143)
K 4.1 mmol/L    (3.4-5.0)
Urea 3.7 mmol/L    (2.5-6.5)
Cr 49 umol/L    (<90)

Venous blood gas

pH 7.37    (7.32-7.42)
PCO2 42 mmol/L    (37-50)
HCO3 24 mmol/L    (22-28)
Cl 96 mmol/L    (96-109)
glc 7.2 mmol/L    (3.0-5.4)
lac 1.9 mmol/L    (<1.5)

FBC and LFTs were normal.

Questions

Q1. What are the laboratory abnormalities and how do they relate to his presentation?

The laboratory findings are:

  • Hyponatremia (123 mmol/L)
  • Borderline low chloride — chloride may be lost due to vomiting.
  • Mildly increased lactate — hyperlactemia is typically found following a seizure, in this case it may actually be normalising after the first seizure
  • Mildly increased glucose — glucose is commonly elevated after a brief seizure, or in the early stages of status, due to a catecholamine-mediated ’stress response’.

Symptoms of hyponatremia do not necessarily correlate well with the degree of hyponatremia. According to UpToDate.com expected symptoms are typically:

<125-130 mmol/L – nausea and malaise
<115-120 mmol/L – headache, lethargy, obtundation, seizures, coma, respiratory arrest, noncardiogenic pulmonary edema.

However, significant symptoms may be found at higher levels depending on the ‘starting concentration’ and the rate of decrease.

For instance, worse symptoms are more likely if sodium rapidly drops from 140 mmol/L to 125 mmol/L than if there is a slow decrease from 130 mmol/L to 115 mmol/L.

Q2. How can you determine if the laboratory abnormality identified in Q1 is contributing to the patient’s symptoms?

Determine if the patient’s neurological status improves by increasing his plasma sodium (and osmolality).

The child was administered 3mL/kg of 3% normal saline over 30 minutes. Immediately following this infusion he was alert with a GCS 15 and had no further vomiting. His only complaint was a mild headache that improved with paracetamol.

This response to treatment suggests (but does not prove) that he was significantly symptomatic with a plasma sodium of 123 mmol/L.

Finally, it is important to remember is that hyponatremia is not a diagnosis – we still don’t know whys he was hyponatremic.

Q3. Is it safe to perform the measure taken in Q2?

There may be a reluctance to administer hypertonic saline due to the fear of the dreaded complication of cerebral pontine myelinolysis (perhaps better called osmotic demyelination syndrome – more than the pons may be involved). This complication may occur with the excessive correction of hyponatremia in patients that have chronic severe hyponatremia (e.g. Na 110-115 for at least 2 days).

Chronicity is important because the brain adapts to hyponatremia by extruding intracellular osmolytes to guard against cerebral edema. The adaptation process occurs over about 2 days, and until it occurs correcting hyponatremia is safe.

In acute symptomatic hyponatremia the risk of osmotic demyelination syndrome from rapid correction of hyponatremia is minimal.

Hypertonic saline should be administered to patients with significant symptoms (e.g. altered mental state, seizures, coma, noncardiogenic pulmonary edema) of hyponatremia, regardless of the sodium level. Usually the aim is to increase the sodium by 1-1.5 mmol/h for 2 or 3 hours, and a small rise can markedly improve symptoms.

In general, sodium should not be increased by more than 10-12mmol over 24h, and 18 mmol/L over 48h. Lower rates are advised for high risk patients (e.g. chronic hyponatremia in the context of malnutrition, alcoholism or advanced liver disease)

The daily rate of increase is more important than the hourly rate, in terms of risk of osmotic demyelination syndrome. So, once the symptoms have improved the rate of correction should be slowed.

—

Further laboratory test results were obtained:

Serum cortisol 1100 nM    (60-420)
TFTs were normal
Osmolality plasma 265 mmol/kg L    (275-295)
Spot urine sodium 209 mM
Spot urine osmolality 681 mmol/kg    (50-1200)

Q4. What do these test results suggest?

These results are consistent with the syndrome of inappropriate anti-diuretic hormone secretion (SIADH).

ADH (aka vasopressin) promotes water reabsorption from the collecting ducts of the kidney by activating the vasopressin V2 receptor. This stimulates the translocation of aquaporin-2 water channels from intracellular sites to the luminal membranes of the principal cells of the collecting duct. The end result is concentrated ‘water-poor’ urine and dilute ‘water-rich’ blood.

Features of SIADH include:

  • Low plasma osmolality
  • urine osmolality > plasma osmolality (usually >300-400 mosmol/kg)
  • Urine sodium concentration usually >40 meq/L
  • Normal acid-base and potassium balance
  • Normal renal, liver, adrenal and thyroid function
  • Diuretics are not in use
  • improves with water restriction

Although these results are suggestive of SIADH, we still do not have the underlying diagnosis… what is the cause of this ‘SIADH’?

Q5. What are the possible causes in this case?

The possible causes of SIADH include:

  • Any CNS disorder –
    stroke, hemorrhage, infection, trauma, and psychosis
  • Pulmonary disorders –
    lung cancer, pneumonia, bronchiolitis, pneumothorax, asthma, etc.
  • Ectopic ADH secretion by a tumour –
    lung cancers (especially small cell lung cancers), and less commonly:
    cancer of the duodenum or pancreas, head and neck cancer, and olfactory neuroblastomas
  • Major surgery –
    especially thoracic or abdominal.
  • Drugs –
    many drugs, including:
    SSRIs, ecstasy, antipsychotics like haloperidol, antiepileptics (e.g. valproate and carbamazepine), MAOIs, NSAIDs, opiates, chemotherapy (e.g. cyclophosphamide, vincristine), amiodarone, bromcriptine, ciprofloxacin…

However, the child in this case did not have SIADH…

Some conditions may mimic SIADH. These include:

  • Hereditary vasopressin receptor abnormalities (‘nephrogenic SIADH’)
  • Cerebral salt wasting (classically in neurological disorders such as subarachnoid haemorhage – it resembles SIADH but the patient is hypovolemic and is responsive to normal saline rather than water restriction)
  • Exogenously administered vasopressin agonists such as vasopressin, desmopressin and oxytocin.

Do you remember from the history that this child had problems with enuresis?

The child had started using a nightly nasal spray of desmopressin to treat his enuresis about 4 days prior to his ED presentation. This exogenously administered analogue of ADH resulted in hyponatremia mimicking SIADH, probably exacerbated by increased water intake prior to his sports competition.

Over the next 12-24 hours he had a large diuresis and his laboratory values all normalized.

References and Links

Filed Under Blood Results, Clinical Case, Emergency Medicine, Intensive Care, Neurology, Pediatrics, Urinalysis Tagged With desmopressin, hypertonic saline, hyponatremia, osmolality, seizure, SIADH

Cardiovascular Curveball #005

March 10, 2010 By Chris Nickson 3 Comments

One of your patients is a 58 year-old man who had a quadruple coronary artery bypass earlier in the day. He had poor cardiac output after the procedure and required the insertion of an intra-aortic balloon pump (IABP) to augment his cardiac function. The medical students on your team have a few questions for you concerning IABPs.

Can you answer them?

Questions

Q1. What is an intra-aortic balloon pump (IABP) and how does it work as a circulatory assist device?

The IABP has two parts:

(1) a large bore catheter with a long sausage-shaped balloon at the distal tip, and

(2) a console containing a pump that inflates the balloon.

The balloon is designed to sit in the proximal descending aorta. It comes in various lengths according to body height, with balloon volumes of about 30-50 mL. The balloon is usually filled with helium gas, and when inflated should fill up 80-90% of the aortic diameter.

The IABP works by inflating and deflating at different phases of the cardiac cycle. Balloon inflation augments diastolic blood pressure and balloon deflation decreases afterload during systole .

IABP effects on aortic pressures

IABP effects on the aortic pressure cycle. The dicrotic notch immediately precedes point C. Key: A. Unassisted End Diastolic Pressure, B.Unassisted Systolic Pressure, C.Unassisted Diastole, D. Reduced Systolic Pressure, E. Diastolic Augmentation, F. Assisted End Diastole Pressure (the unlabeled arrow!) (from www.ecp-india.net)

Balloon inflation in early diastole (usually triggered by the R wave on the ECG) increases diastolic blood pressure (E). This in turn increases systemic perfusion and coronary perfusion (at least in the hypotensive patient). Balloon inflation thus displaces blood both proximally and distally. The increase in coronary perfusion increases myocardial oxygen supply.

Balloon deflation occurs at the end of diastole resulting in a decreased end diastolic blood pressure (F). This reduces the aortic pressure at the start of systolic ejection, thus decreasing the afterload that the heart has to pump against. This decreases myocardial oxygen demand and improves systemic perfusion during systole.

This animation may help in visualising how the IABP works (bear with the funky accent! – you may need to increase the volume):

embedded by Embedded Video

YouTube Direkt

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Q2. What are the indications for IABP use?

The IABP can be used whenever there is cardiac pump failure if:

  • it may resolve spontaneously, or
  • a corrective procedure is planned.

In other words, there has to be some hope of the patient being able to survive without an IABP in the future.

Some situations where an IABP is used include:

  • Cardiogenic shock after coronary artery bypass grafting (CABG) or acute myocardial infarction
  • unstable angina
  • Acute mitral incompetence
  • Planned cardiac transplant
  • ventricular arrhythmias refractory to conventional treatment
  • cardiotoxicity from poisoning, e.g. verapamil overdose

—

Q3. How is an IABP inserted and positioned?

IABPs are usually inserted using the Seldinger technique via the femoral artery so that the tip of the catheter is advanced proximally into the aorta. Fluoroscopy is not essential for insertion, so an IABP can be placed emergently.

IABP’s must be appropriately positioned:

The balloon tip is positioned just distal to the origin of the left subclavian artery, and the entire balloon should lie above the renal arteries.

Here is a more detailed description of the steps involved in IABP insertion as described by Charles Gommersall:

  1. heparinise patient prior to insertion of catheter providing there are no contraindications such as recent surgery.
  2. prep skin
  3. fully collapse balloon applying 30 ml vacuum with 60 ml syringe
  4. insert needle into femoral artery at 45° and pass it through both walls of artery. Withdraw needle until strong pulsatile jet of blood is obtained
  5. pass guidewire through needle and advance until tip is is in thoracic aorta. Wire should pass very easily
  6. pass sheath over wire in similar manner to insertion of PA catheter sheath
  7. pass balloon over guidewire through sheath. Must be inserted to at least the level of the manufacturer’s mark (usually double line) to ensure that entire balloon has emerged from sheath
  8. balloon should be positioned so that the tip is about 1 cm distal to the origin of the left subclavian artery. If fluroscopy is not available during insertion the distance from the angle of Louis down to the umbilicus and then to the femoral artery insertion site should be measured to approximate the distance the balloon should be advanced and the position should be checked on CXR
  9. remove wire. Return of blood via central lumen confirms that the tip is not subintimal and has not caused a dissection.
  10. flush central lumen with heparin saline and connect to transducer to monitor intra-aortic pressure (the outer lumen transmits helium gas to the balloon)
  11. monitor Doppler ankle pressures and compare with preinsertion value

Note: once the balloon has been inflated, even if it is then deflated, it must not be removed through the sheath for any reason – the sheath must be removed first.

—

Q4. When is an IABP contra-indicated?

Contra-indications include:

  • Aortic insufficiency
  • Aortic dissection
  • Patent ductus arteriosus
  • Severe peripheral vascular disease
  • Thoracic aortic graft <12 months old
  • the patient’s cardiac index is too low for there to be a clinical benefit from IABP assistance

—

Q5. What are the determinants of IABP efficiency?

IABP efficiency is determined by:

  • Timing of balloon inflation and deflation
  • Assist ratio (e.g. 1:1 – balloon inflation and deflation on every cardiac cycle – provides greater circulatory assistance than 1:2 or 1:4 – balloon inflation and deflation on every 2nd or 4th cardiac cycle )
  • Heart rate (efficiency is greatly decreased at heart rates >130/min)
  • Gas loss from balloon (balloon volume)
  • Minimum cardiac index of 1.2 – 1.4 L/min/m2 is required for IABP assistance to be clinically beneficial

—

Q6. How can IABP function be optimised?

Optimisation can be achieved by ensuring that:

  • inflation of the balloon occurs at the dicrotic notch (forming the ‘V’)
  • the slope of rise of augmented diastolic waveform is straight and parallel to the systolic upstroke
  • the augmented DBP at balloon deflation exceeds or is equal to end-systolic BP
  • the end-diastolic BP at balloon deflation is lower than the preceding unassisted end-DBP by 15-20 mmHg
  • the assisted SBP (following a cycle of balloon inflation) is lower than the previous unassisted SBP by 5 mmHg

—

Q7. What are the complications of IABPs?

Complications can occur during insertion, while the IABP is in use, during removal, or after removal.

During insertion

  • failure to advance catheter beyond iliofemoral system because of atherosclerotic disease (common)
  • aortic dissection and arterial perforation – may cause retroperitoneal hemorrhage.

During use

  • Ischemia
    • ischemia of the lower limbs (up to 25% of all IABP patients)
      • may occur while the IABP is in place, or hours after removal due to thromboembolic showers
      • ischemia usually results from thrombosis at the insertion site
      • Can affect contra-lateral leg due due to cholesterol emboli and thromboembolic showers from the balloon
      • Close neurovascular monitoring essential – sensorimotor loss generally mandates removal
      • Pulseless limb may need to be tolerated if IABP is life-saving
    • Visceral ischemia
    • Spinal ischemia
  • Balloon rupture causing helium embolus
      • this may be heralded by high balloon inflation pressures.
      • The key indicator of balloon rupture is the presence of blood in the connecting tubing.
      • Management involves immediate cessation of counterpulsation, placement of the patient head down and IAB removal. Consider giving broad spectrum antibiotics as the gas chamber of the balloon is not sterile.
  • Hemolysis and consumptive thrombocytopenia
  • Peripheral neuropathy
  • Catheter-related infection
  • Small perforation in balloon membrane
    • this may allow a small amount of blood to leak into balloon lumen. The blood is dessicated by the dry helium and forms a hard pellet which may stop the balloon from being removed without surgical aortotomy.

During or after removal:

  • Haematoma
  • Pseudoaneurysm
  • AV fistula

—

References and Links

  • Datascope’s IABP elearning modules
  • Gomersall C. Intra-aortic balloon pumping. 1999.
  • Krishna M, Zacharowski K. Principles of Intra-Aortic Balloon Pump Counterpulsation. Cont Edu Anaesth Crit Care & Pain. 2009;9(1):24-28.
  • Life in  the Fast Lane: Paul Young’s ICU Mind Maps – Intra-Aortic Balloon Pump [pdf]
  • Marino PL. The ICU Book (3rd edition). 2007; Wolters Kluwer.
  • Overwalder PJ. Intra Aortic Balloon Pump (IABP) Counterpulsation. The Internet Journal of Perfusionists. 2000;1:(1) (fulltext online)
Filed Under Cardiology, Clinical Case, Intensive Care, Procedure Tagged With cardiogenic, circulatory assist device, critical care, IABP, intra-aortic balloon pump, shock

Acute Severe Asthma

March 9, 2010 By Kane Guthrie 3 Comments

A 25-year-old lady Miss. Poor Compliance is rushed into your Emergency Department as a Priority 1. She is a brittle asthmatic and has been given 3x 5mg salbutamol nebs, and 0.5mg of adrenaline IM prehospital. On arrival Miss PC is sitting forward in the tripod position, using her accessory muscles to breath. She is tachypnoeic, agitated and unable to talk.

Vital signs: Pulse 143, BP 138/95, RR 42, Sp02 91% on neb, GCS 14/15.

Past Medical and Medication History

Asthma Epidemiology

  • Over 2.2 million Australians have currently diagnosed asthma
  • 406 deaths attributed to asthma in 2006
  • Highest risk of dying from asthma is in the elderly over 70
  • The emergency clinician’s goal in treating acute severe asthma is preventing intubation
  • Severe/Critical asthma is a life threatening condition

Asthma Pathophysiology

  • Asthma is a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role, in particular, mast cells, eosinophils, T lymphocytes, macrophages, neutrophils, and epithelial cells.
  • The inflammation in asthma cause recurrent episode of wheezing, breathlessness, chest tightness, and coughing. Airflow obstruction in asthma is the result of contraction of the airway smooth muscle and swelling of the airway wall due to:
    • Smooth muscle hypertrophy and hyperplasia
    • Inflammatory cell infiltration and oedema
    • Goblet cell and mucous gland hyperplasia with mucous hypersecretion
    • Protein deposition including collagen
    • Epithelial desquamation
  • Near fatal asthma  (NFA) is described as acute asthma associated with a respiratory arrest or arterial carbon dioxide level greater than 50mmHg, with or without altered conscious state. Two distinctive phenotypes of NFA have been identified:
    • Most common, responsible for 80-85% of all fatal events is characterised by eosinophilic inflammation associated with gradual deterioration over days-weeks occurring in patients with severe or poorly controlled asthma, and is slow to respond to therapy.
    • The second phenotype, with neutrophilic inflammation, has both rapid onset and response to therapy.

Markers of severe asthma:

justbreathe1 266x300 Acute Severe Asthma

Acute Severe Asthma is Scary for the Patient

  • End of the bed test:
    • Inability to speak in full sentences
    • Use of accessory muscles or tracheal tugging
    • Cyanosis and sweating
  • Clinical Signs:
    • Pulsus paradoxus (>15mmHg decreased with inspiration). With severe muscle fatigue might be absent
    • Quiet chest on auscultation (The “Silent Chest”)
    • Confusion or decreased level of consciousness
    • Hypotension or bradycardia
  • Objective measurements:
    • FEV 1<40% predicted
    • PEF <40% of predicted or best (<25% in life threatening asthma)
    • Oxygen saturation <90-92%
    • PaO2 <60mmHg
    • PaCO2 >45mmHg

Complications of Asthma:

  • Pneumothorax, Pneumomediastinum, Pneumopericardium and Pneumoretroperitoneum
  • Cardiac Arrhythmias, Myocardial ischaemia or infarction
  • Electrolyte disturbances (hypokalaemia, hypomagnesaemia, hypophosphataemia)
  • Lactic Acidosis
  • Hyperglycaemia
Pneumomediastinum asthma 2 s Acute Severe Asthma

Pneumomediastinum in asthmatic

Conditions that may mimic acute asthma:

  • Upper airway obstruction
  • Foreign-body aspiration
  • Vocal cord dysfunction syndrome
  • Pulmonary oedema
  • Acute exacerbations of COPD
  • Hysterical conversion reaction
  • Munchausen syndrome
Pneumomediastinum asthma s Acute Severe Asthma

Pneumomediastinum

Diagnostic Test:

  • Chest X-Ray
    • Hyperinflation 5-10%
    • Infiltrate 5%
    • Pneumothorax <1%
    • Pneumomediastinum <1%
  • Arterial Blood Gas
    • Respiratory alkalosis typical
    • Inaccurate predictor of outcome
    • Will seldom alter your treatment plan
    • Painful
  • Peak Flow
    • An objective measure of lung function
    • Useful to assess response to treatment
    • Impossible to obtain in the dying patient
    • PEFM Measurements:
      • <25% Severe
      • 25-50% Moderate
      • 50-70% Mild
      • >70% Discharge Goal
  • Pulse Oximetry
    • Simple, and less painful than ABG
    • Provides continuous oxygenation measurements
    • Needs to placed on well-perfused site, difficult to obtain readings if global hypoperfusion or peripheral vasoconstriction present.
    • Aim to keep sp02 >92%

Management of Acute Severe Asthma

Oxygen:

  • Hypoxia is the main cause of death in asthma
  • Oxygen should be given to keep Sp02 above 92%
  • A slight Pco2 rise may occur with oxygen therapy but this is of no clinical significance.

Beta-agonists:

  • Rapid acting inhaled beta-agonists (bronchodilators) are the first line therapy for acute asthma.
  • Nebulisers should generally be used in acute severe asthma, as provide easier delivery of medication to patient, multi dose inhalers have a role in mild to moderate asthma.
  • IV salbutamol gives you the advantage of hitting the beta 2 receptors from the back door, while continuing nebulizer treatment, and should be trialed in patients not responding to nebulisers.
  • Continuous nebuliser therapy appears to be more effective than intermittent nebulisers for delivering beta-agonist drugs to relieve airway spasm in acute severe asthma.  (Cochrane Review, 2009)
  • Salbutamol toxicity can caused a lactic acidosis which is often unrecognized in asthma patients, the lactic acidosis has been hypothesized to adversely affect ventilation by increasing ventilatory demand, increasing dead space ventilation, worsening dynamic hyperinflation and intrinsic PEEP. Management is to discontinue salbutamol at the earliest opportunity.
  • Hypokalaemia will occur with continuous beta-agonist use, and potassium replacement should occur early in the treatment course.
    • Dose:  Salbutamol Nebuliser Ampoule 5mg
    • Dose: Salbutamol IV 5mg in 500mL of 0.9% sodium chloride or 5% dextrose start at 30mL/hr titrating up to 120mL/hr

    Anticholinergics:

    • Anticholinergics agents block muscarinic receptors in airway smooth muscles, inhibit vagal cholinergic tone and result in bronchodilation.
    • Ipratropium bromide is the most common agent added to beta-agonist in the treatment of acute severe asthma.
      • Dose: Ipratropium bromide (Atrovent) 500ug to second dose of salbutamol via neb, can be repeated every 4hours

    Steroids:

    • Use of corticosteroids within 1 hour of presentation to an ED significantly reduces the need for hospital admission in patients with acute asthma. Benefits appear greatest in patients with more severe asthma, and those not currently receiving steroids
    • Corticosteroids work by targeting airway oedema and secretions associated with acute asthma through their anti-inflammatory actions
      • Dose: Prednisolone 50mg PO
      • Dose: IV Hydrocortisone 100-200mg
      • Note: Parenteral route is indicated in ventilated patient or patient unable to swallow, eg. Vomiting

    Adrenaline:

    • Can be give either intravenously or via nebulizer
    • Bronchoconstriction is the major pathology in asthma; airway oedema might also make a significant contribution. Both the a-agonist and B-agonist effects of adrenaline might be beneficial, with the alpha effect decreasing oedema and the beta effect responsible for bronchodilation.
    • Adrenaline is generally used, as a rescue therapy in severe asthma complicated by hypotension that is not secondary to dynamic hyperinflation.
      • Dose:  IV 6mg in 100mls 5% dextrose start at 1-15mLs/hour
      • Dose: Nebulizer 1mg in 3ml normal saline

    Aminophylline:

    • The popularity of aminophylline in asthma exacerbations has diminished in recent years.
    • Systematic reviews have shown that IV aminophylline in severe acute asthma does not produce additional bronchodilation above that achieved with beta-agonist and corticosteroids.
    • Side effects; cardiac arrhythmia’s, vomiting, toxicity.
    • Need to check Theophyline level if patient already taking
      • Dose: 5mg/kg over 20min followed by infusion of 500mg aminophyline n 500mL of 5% dextrose at 0.5mg/kg per hour

    Magnesium Sulphate:

    • Magnesium potential role is asthma may involve a combination of smooth muscle relaxation, inhibition of histamine release and acetylcholine release from nerve endings.
    • Most evidence to support the use of magnesium in asthma is in the acute severe asthmatic were it has been shown to be safe and beneficial.
    • Magnesium should be trialed when the patient is not responding to bronchodilator therapy.
      • Dose: IV 2-4mg of 30-60mins

    Heliox:

    • Heliox Mixture 80% helium/20% oxygen
    • There is evidence that helium and oxygen mixtures (heliox) may provide additional benefits to patients with acute asthma.
    • Heliox mixtures have the potential to decrease airway resistance, and therefore decrease the work of breathing for the severe acute asthma patient.

    Antibiotics:

    • Antibiotics are not indicated in the management of severe acute asthma.
    • Antibiotics should only be used in the setting of an underlying pneumonia, respiratory tract infection or to aid in the prevention of ventilator-associated pneumonia in ICU.

    Airway Management

    Non-Invasive Positive Pressure Ventilation:

    Good quality evidence and trails to support the use of NPPV in asthma are lacking, however it is worth trying when intubation is not immediately indicated. Remember the goal of the emergency clinician’s in treating asthma is to prevent intubation.

    • Positive pressure is generally less than 15cmH2O
    • Benefit between CPAP vs BiPAP is unknown
    • Tachypnea caused by severe asthma can make it difficult for the patient to coordinate they’re breathing with machine making BiPAP uncomfortable
    • Need a large randomised control trial to determine the effectives properly of NIV, in acute severe asthma.

    embedded by Embedded Video

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    “Asthmatic on BiPAP before being Intubated”

    Mechanical Ventilation:

    1-3% of acute severe asthma requires intubation. Prevention of intubation and mechanical ventilation are the goals of managing acute severe asthma, this can be achieved by maximising pre-intubation therapy, however you don’t want to wait too long or let the severe asthmatic tire before trying to intubate them. Once an asthmatic is intubated and ventilated their morbidity and mortality increasing dramatically, and it can be difficult to wean from the ventilator.

    Criteria for Intubation:

    • Clinical Indicators:
      • Cardiac or Respiratory arrest
      • Altered mental status
      • Progressive exhaustion
    • Laboratory Indicators:
      • Severe hypoxia despite maximal oxygen delivery
      • Failure to reverse severe respiratory acidosis despite intensive therapy
      • pH <7.2, carbon dioxide pressure increasing by more than 5mmHg/hr or greater than 55 to 70mm/Hg, or oxygen pressure of less than 60mm/Hg.

    Challenges:

    • Effective pre-oxygenation impossible
    • No margin for error or delay
    • Need to be intubated by most experienced person available
    • High intrathoracic pressure after RSI

    Recommendations:

    • Fluid bolus before intubation if possible
    • RSI preferred
    • Ketamine for bronchodilator effects
    • Permissive hypercapnea essential

    Initial Ventilator settings in paralysed patients:

    • FiO2 1.0, then titrate to keep SpO2 >94%
    • Tidal Volume 5-6ml/kg
    • Ventilator rate 6-8 breaths/min
    • Long expiratory time (I:E ratio >1:2)
    • Minimal PEEP < 5cmH2O
    • Limit peak inspiratory pressure to <40cmH2O
    • Target plateau pressure <20cmH2O
    • Ensure effective humidification

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    References

    Brenner, B. Corbridge, T. & Kazzi, A. (2009). Intubation and mechanical ventilation of the asthmatic patient in respiratory failure. The Journal of Emergency Medicine. 37(2s), s23-s34.

    Camargo, C. Rachelefsky, G. & Schatz, M. (2009). Managing Asthma Exacerbations in the Emergency Department: Summary of the National Asthma Education and Prevention Program Expert Panel Report 3 Guidelines for the Management of Asthma Exacerbations.The Journal of Emergency Medicine. 37 (2S), S6-S17.

    Camargo, C. Spooner, C. & Rowe, B. (2009). Continuous versus intermittent beta-agonist for acute asthma (Review). http://www.thecochranelibrary.com.

    Chua, F. & Lai, D. (2007). Acute severe asthma: Triage, treatment and thereafter. Current Anaesthesia & Critical Care. 18, 61-68.

    Creagh-Brown, B. & Ball, J. (2007). An under-recognized complication of treatment of acute severe asthma. American Journal of Emergency Medicine. 26, 513-515.

    Hodder, R. et al. (2009). Management of acute asthma in adults in the emergency department: nonventilatory management.  CMAJ. 182(2), E55-E67.

    Holley, A. & Boots, R.(2009). Review article: Management of acute severe and near-fatal asthma. Emergency Medicine Australasia, (21) 259-268.

    Jones, L. & Goodacre, S. (2009). Magnesium sulphate in the treatment of acute asthma: evaluation of current practice in adult emergency departments. Emergency Medicine Journal. 26, 783-785.

    Melnick, E. & Cottral, J. (2010). Current Guidelines for Management of Asthma in the Emergency Department.  http://www.ebmedicine.net. 2(2). 1-13.

    Morris, F. & Fletcher, A. (Ed). (2009). ABC of Emergency Differential Diagnosis. Oxford: Blackwell Publishing

    National Asthma Council of Australia. Asthma management handbook: 2006. Accessed http://www.nationalasthma.org.au/cms/images/stories/amh2006_web_5.pdf, 12/02/2010

    Nowak, R. Corbridge, T. & Brenner, B. (2009). Noninvasive Ventilation. The Journal of Emergency Medicine. 37(2S), S18-S22.

    Peters, S. (2007). Continuous Bronchodilator Therapy. Chest. 131(1),1-5.

    Phipps, P. & Garrard, C. (2003). The pulmonary physician in critical care. 12: Acute severe asthma in the intensive care unit. Thorax. 58, 81-88.

    Ram, F. Wellington, S. Rowe, B. & Wedzicha, J. (2009). Non-invasive positive pressure ventilation for treatment of respiratory failure due to severe acute exacerbations of asthma (Review). http://www.thecochranelibrary.com.

    Rodrigo, G. Pollack, C. Rodrigo, C. Rowe, B. (2010). Heliox for non-intubated acute asthma patents (Review). http://www.thecochranelibrary.com.

    Rowe, B. Spooner, C. Ducharme, F. Bretzlaff, J. Bota, G. (2008). Early emergency department treatment of acute asthma with systemic corticosteroids (Review). http://www.thecochranelibrary.com.

    Rowe, B. et al. (2009). Magnesium sulfate for treating exacerbations of acute asthma in the emergency department (Review). http://www.thecochranelibrary.com.

    Filed Under Emergency Medicine, Intensive Care, Respiratory, lecture notes Tagged With Acute Severe, asthma, Near Fatal Asthma, Status Asthmaticus

    Clinical Images Online

    February 22, 2010 By Chris Nickson 10 Comments

    The internet era gives clinicians unprecedented access to clinical images for learning and teaching purposes – and no matter how old some of us may be, we all remain students until the end.

    Here are some useful clinical image collections for use primarily by doctors in emergency medicine and intensive care medicine. Of course, we being disciples of the ‘Open Source Messiah’, the emphasis is firmly on free-to-use resources. An updated index will be maintained here.

    Clinical Image Collections Online

    Clinicalcases.org – The definitive online case-based medical learning website includes links to the best images from some of the major general medical journals -especially the NEJM, Lancet and BMJ. The site is organised by specialty with a link to the images below the lists of cases. Here are the clinical image specialty links for ready reference:

    Cardiology — Endocrinology — Gastroenterology — Hematology and Oncology — Infectious diseases — Nephrology — Neurology — Pulmonology and Critical Care — Rheumatology

    Catalog of Clinical Images – UCSD’s high quality collection of photographs of physical examination findings by anatomical region.

    Trauma Image Database – A categorized collection of trauma-related images from Trauma.org.

    PhotoRounds – Brief ‘test yourself’ clinical images best viewed as ‘unknowns’.

    Eye Atlas Online – A beautifully presented database of images of eye diseases crafted in Italy.

    DermisNet, DermNet, and DermNet NZ – Being such a visually-orientated specialty it is not surprising that there are an abundance of quality dermatology image collections out there. These are my favourites for when I need to clinch a diagnosis of ‘aplasia cutis congenita circumscripta‘…

    Life in the Fast Lane – VAQs and Clinical Cases and Case-based Q&As.

    Clinical Images from Medical Journals

    No journal subscriptions are needed to access any of these resources:

    NEJM Featured Images in Clinical Medicine – the classic web-only series from the New England Journal of Medicine – alternatively, try the addictive NEJM Image Challenge.

    CMAJ Clinical Images – The search results for ‘clinical images’ – open access classic, dramatic or note-worthy clinical images from the journal of the Canadian Medical Association.

    Clinical Pearls: Photographic Case Reports – a collection from the journal Academic Emergency Medicine.

    Diagnosis at a Glance – The entire series from Emergency Medicine.

    Images in Emergency Medicine – Much of this collection of images from this series in the Annals of Emergency Medicine can be accessed free online.

    Clinical Imaging – Radiology and Ultrasonography

    Emergency medicine-orientated:

    EMPACS – Emergency Medicine Picture Archiving & Communication System – This is an impressive resource providing annotated images relevant to emergency settings from all modalities (USS, XR, CT, MRI, etc). Registration is free and all images may be reused if appropriately referenced to empacs.org. It even features a quiz mode.

    On Call Radiology – A set of teaching files to identify common radiology findings on call and in the Emergency room. The site includes an image catalogue.

    The Image Browser from the excellent Ultrasound Guide for Emergency Medicine – Not many images, but too cool to leave out. The image browser is only a small part of the best online resource for emergency medicine ultrasound currently available (reviewed here on LitFL).

    Other radiology resources:

    Cases from The Radiology Assistant – This Dutch website is impressive… Its a great way to learn radiology.

    LearningRadiology.com – There is a massive ‘Case of the Week’ archive as well as an image index.

    Interpretation of the ICU Chest Film – An excellent beginner’s guide to to the sometimes bewildering chest film in intensive care.

    Pediatric radiology resources:

    Radiology Cases in Pediatric Emergency Medicine – an aging but otherwise impressive set of teaching files from the University of Hawaii.

    Pediatric Radiology – A collection of annotated images from the Cleveland Clinic that covers the core curriculum required for pediatric radiologists.

    Pedrad.info – Pediatric Radiology information, publication and communication platform. Includes an Index, Case of the Day and Most Interesting Cases.

    Pathology, Microbiology and Parasitology

    PathWeb – it is no small mercy for docs in the ED and ICU that we rarely have to look pathological specimens, but if you ever need to, this massive database is a good place to go.

    DPDx Parasite Image Library – A superbly presented collection of parasite images from the CDC.

    Malaria – An excellent resource from Royal Perth Hospital for learning how to identify malaria parasites on blood films.

    If you know of other image-based web resources that deserve to be on this list please leave a comment below!

    Filed Under Emergency Medicine, Featured, Intensive Care, Investigation [tests], Radiology, VAQ, eLearning Tagged With clincal image, Dermatology, Emergency Medicine, Eye, Intensive Care, microbiology, pathology, physical examination, Radiology, Ultrasound

    Pediatric Perplexity #001

    February 9, 2010 By Chris Nickson 4 Comments

    A 7 year-old girl was brought to hospital with sudden onset vomiting followed by lethargy and irritability. A week previously she developed chicken pox and was recovering well, having been treated with regular aspirin and paracetamol for fever and discomfort. There is no history of any other drug or toxin exposure and no family history of childhood diseases. When you review her she is afebrile, anicteric, drowsy and mildly dehydrated. She has mild hepatomegaly on palpation. She has no focal neurological deficits. Relevant findings on her investigations include:

    • Lumbar puncture — CSF essentially normal (WBC 2 x 109/L)
    • CT head — suspicious for mild cerebral edema
    • Metabolic screen — no evidence of any inborn error of metabolism (IEM), normal urinary copper excretion
    • Blood tests — hyperammonaemia (NH3 210 micromol/L) and abnormal LFTs (ALT 1150 IU/L). An initial mild hypoglycemia was corrected with glucose administration.

    Questions

    Q1. What is the likely diagnosis?

    Reye syndrome

    Reye syndrome is an acute metabolic encephalopathy associated with hepatic dysfunction characterized by ‘fatty metamorphosis’. It was named after the Australian doctor who described it in 1963 and has a mortality rate of about 20-40%. It is has been an extremely rare diagnosis since the 1980s. The disappearance of Reye Syndrome is attributed to our increased ability to diagnose IEMs that cause Reye-like syndromes and successful public health campaigns to stop the use of aspirin in children with febrile illnesses. Reye syndrome hardly ever affects adults.

    —

    Q2. What are the CDC’s diagnostic criteria for this condition?

    The CDC’s 1990 clinical case definition for Reye Syndrome is ‘an illness that meets all of the following criteria’:

    • Acute, noninflammatory encephalopathy that is documented clinically by:
      • an alteration in consciousness and, if available,
      • a record of the CSF containing less than or equal to 8 leukocytes/cu.mm or a histologic specimen demonstrating cerebral edema without perivascular or meningeal inflammation
    • Hepatopathy documented by either:
      • a liver biopsy or an autopsy considered to be diagnostic of Reye syndrome or
      • a threefold or greater increase in the levels of the serum glutamic-oxaloacetic transaminase (SGOT), serum glutamic-pyruvic transaminase (SGPT), or serum ammonia
    • No more reasonable explanation for the cerebral and hepatic abnormalities

    —

    Q3. What are the clinical features of this condition?

    Findings on the history include:

    • Recent viral illness or vaccination
      — especially influenza A or B, and varicella zoster (chicken pox).
    • Recent salicylate use (e.g. aspirin)
      — over 80% of cases report aspirin use in the previous 3wks
    • Vomiting
      — often with an abrupt onset within few days (12h to 3 weeks) of the resolution of the viral illness
    • Neurological symptoms
      — Onset heralded by repetitive vomiting
      — Lethargy, irritability, restlessness, delirium, seizures, loss of brainstem reflexes, decorticate or decrebrate coma and flaccid paralysis.

    Findings on physical examination include:

    • Protracted vomiting ± dehydration
    • Afebrile with encephalopathy (see neurological symptoms)
    • hepatomegaly (~50%) but with minimal or absent jaundice

    The severity of Reye syndrome is described using a 6 stage classification ranging from 0 (alert, wakeful) to V (flaccid non-responsive coma).

    Clinical course of Reye Syndrome

    Clinical course of Reye Syndrome (from Sarnaik, 1999). Click to enlarge.

    —

    Q4. What is the cause of this condition? How is aspirin involved?

    The exact mechanisms leading to Reye syndrome are obscure.

    It is thought to result when a sensitized virus-infected host is exposed to an agent that causes mitochondrial dysfunction.

    This combination of insults leads to inhibition of oxidative phosphorylation and fatty-acid beta-oxidation and the resulting metabolic derangement manifests as neurological and hepatic dysfunction. The most important precipitating agents is thought to be:

    Aspirin (and other salicylates)

    The actions of the CDC and FDA in the early 1980’s led to the widespread banishment of aspirin from general use in children. Some experts still question whether aspirin has a causal role in the disorder as not every case of Reye syndrome involves aspirin exposure and only about about 1/1000 children using aspirin get the disorder. In my view, however, the relative disappearance of this terrible disease since the discontinuation of widespread aspirin use in children should not be trivialized. Other drugs and toxins might also act as triggers of mitochondrial dysfunction — paracetamol, valproate, and antiemetics have all been cited as potential culprits.

    —

    Q5. Describe appropriate management of this child?

    There is no specific treatment for Reye syndrome.

    Standard supportive care and monitoring should be provided, generally in an ICU-level setting.

    • Attend to ABCs
    • Treat hypoglycemia
    • Treat seizures — e.g. benzodiapines, phenytoin
    • Treat vomiting — antiemetics. e.g. ondansetron
    • Appropriate fluid management
    • Correct hyperammonaemia
      • Consider use of ammonia detoxicants (sodium phenylacetate and sodium benzoate) that prevent ammonia production from glycine and glutamine.
    • Prevent and treat raised intracranial pressure
    • Treat severe metabolic acidosis
    • Correct coagulopathy
    • Prevent and treat other potential complications, e.g. sepsis, multiple organ dysfunction syndrome (MODS), SIADH, diabetes insipidus.

    —

    References

    ResearchBlogging.org

    • Glasgow JF, & Middleton B (2001). Reye syndrome — insights on causation and prognosis. Archives of disease in childhood, 85 (5), 351-3 PMID: 11668090
    • Reye RDK, Morgan G, Baral J (1963). Encephalopathy and fatty degeneration of the viscera: A disease entity in childhood. The Lancet, 282 (7311), 749-752 DOI: 10.1016/S0140-6736(63)90554-3
    • Sarnaik AP (1999). Reye’s syndrome: hold the obituary. Critical care medicine, 27 (8), 1674-6 PMID: 10470794
    • Schror K (2007). Aspirin and Reye syndrome: a review of the evidence. Paediatric drugs, 9 (3), 195-204 PMID: 17523700
    Filed Under Clinical Case, Emergency Medicine, Intensive Care, Neurology, Pediatrics Tagged With aspirin, encephalopathy, hepatopathy, liver failure, reye syndrome, viral illness

    Downstairs Patients, Upstairs!

    February 3, 2010 By Chris Nickson 15 Comments

    UCEM have enlisted the help of Dr. Scott Weingart (without his knowledge of course) to improve the care of patients presenting for assessment by Waiting Room Medicine subspecialists.  UCEM’s Chair of Pedantry and resident super-genius, Professor Stickler is almost impressed by Dr. Weingart’s view that hospital geography should not determine the level of care a patient receives:

    “My career goal and the purpose of this blog and podcast are to bring ‘Upstairs Care, Downstairs’ – that is to bring ICU level care to the ED, so our patients can receive optimum treatment the moment they roll through the door.”
    - Scott Weingart, emcrit.org

    However, Professor Stickler has taken this philosophy a step further, ingeniously inverting Weingart’s philosophy of emergency care, so that even greater gains can be achieved. Thus, UCEM is introducing a new policy of ‘Downstairs Patients, Upstairs!’.

    As Professor Stickler’s explains:

    “I had just sent an email to Professor Andrew Wiles suggesting a few subtle corrections to his much feted solution to Fermat’s Last Theorem, when it hit me in an orgasmic wave of synaesthetic bliss like a Kekulian snake eating its own tail… I jumped straight up and out of the bath and thought to myself, “Archimedes, 11000101110102, ha!’.”

    “Clearly the transition of care should not be a one way street. ‘Upstairs Care, Downstairs’ is a moderately impressive concept, but it pales in comparison to my revolutionary ‘Downstairs Patients, Upstairs!” paradigm.”

    Although It may be some decades before the complete ‘Downstairs Patients, Upstairs!’ manifesto is published, UCEM have issued a press release highlighting some of the benefits of transferring patients typically treated in the emergency department straight to the intensive care unit:

    • Is your patient a really mean, sociopathic nasty piece-of-work? Or does your patient just talk too much? Well put up with it no longer… Free-and-easy employment of the endotracheal tube – aka ‘the ultimate personality improvement device’ – brings peace to one-and-all faster than a double dose of UCEM’s new polypill.
    • Sick of all the drunks clogging up your waiting room? Is your patient too intoxicated to be assessed by the psychiatricians? Can’t tell if its the bang on the head or the grog in the blood that’s the problem? Pop in a vascath and fire up the dialysis machine, they’ll be sober in no time.
    • Got problems with patients with gut problems? They’ve got diarrhoea and are due to travel, but are allergic to lomotil? Send them home with a rectal tube and everyone’s happy. Or, you need a stool specimen stat and the patient’s blocked through-flow is blocking the flow through the department? Give ‘em a neostigmine infusion and you’ll have enough specimens to keep Prof Bristol happy for life.
    • Are your patient’s whiskers are an affront to civilized sensibilities? Once in ICU the nurses there will do what they do best: ridding the world of offensive facial hair. If Samuel Johnson was around today he would think differently about which profession is the ‘Greatest Benefit to Mankind‘…
    • Does your patient say they’ve tried everything to lose weight? In ICU they will go straight to Phase 3 of the ELF dietary plan – the ‘Sleeping Beauty’ diet. Warning: may not be effective for somnophages.
    • Does your patient have back pain and is lying around feeling sorry for himself? Get the ICU physiotherapists to work on him – they are renowned for their brutality – sorry, I meant ‘enthusiasm and efficacy’ – he’ll be up and moving in no time. And he’ll be more than happy to be on his way home.

    Of course, there will be a major plus for those working in ICU too, after all, that calm and serene ICU atmosphere could do with a bit of livening up, something to drown out the machines that go bleep…

    UCEM welcomes any and all submissions for inclusion in the ‘Downstairs Patients, Upstairs!’ manifesto.

    Filed Under Emergency Medicine, Featured, Intensive Care, Medical Humor, UCEM Tagged With emcrit, Emergency Medicine, Intensive Care, Medical Humor, scott weingart, UCEM

    Metabolic Muddle #004

    February 2, 2010 By Chris Nickson 5 Comments

    You are asked to review a 73 year old lady who is in hospital for treatment of septic arthritis affecting a prosthetic right hip joint inserted 5 years earlier. The joint has been washed out and debrided twice, and she is receiving IV flucloxacillin and meropenem following culture of a methicillin-sensitive Staphylococcus aureus. She is on regular paracetamol for pain. Unfortunately, she has continued to deteriorate and now has bilateral patchy infiltrates on her chest x-ray. These are her vital signs:

    P 115/min — BP 105/55 mmHg — RR 35/min — SO2 99% on FiO2 0.5 — GCS 12.

    Her UEC and ABG results are shown:

    Sodium (mmol/L) 142 135-145
    Potassium (mmol/L) 3.2 3.5-5.0
    Urea (mmol/L) 18 2.5-7.5
    Creatinine (mumol/L) 140 30-120
    Chloride (mmol/L) 104 95-108
    pH 7.15 7.35-7.45
    PaO2 (mmHg) at FiO2 0.5 100
    PaCO2 (mmHg) 28
    HCO3 (mmol/L) 8 22-28
    Glucose (mmol/L) 6 3.5-6.5
    Lactate (mmol/L) 1.0 <2.0
    b-hydroxybutyrate (mmol/L) 0.15 <0.2
    Osmolar gap (mosm/kg) 9 <12

    [Case description is a modification of Case 1 in Dempsey et al, 2000]

    Questions

    Q1. What is the anion gap?

    Remember that:

    • anion gap = [Na] – ([HCO3] + [Cl])
    • normal anion gap is 2-10 mEq/L

    In this case the anion gap is high:

    • 142 – (8 + 104) = 30 mEq/L

    —

    Q2. Describe the acid-base disturbance.

    Severe acidemia (pH 7.15) resulting from a high-anion gap metabolic acidosis (HAGMA) with incomplete respiratory compensation.

    Incomplete respiratory compensation may due to the presence of bilateral pulmonary infiltrates, exhaustion or obtundation.
    —

    Q3. What is the likely cause of the primary acid-base disturbance and how would you confirm it?

    Remember the causes of HAGMA?

    Given that the lactate and ketones are normal the most likely cause is:

    pyroglutamic acidemia (aka 5-oxoprolinemia)

    This can be confirmed by performing a metabolic screen for urinary organic acids. Blood levels may be required if the patient is anuric. An elevated level of pyroglutamic acid confirms the diagnosis.
    —

    Q4. What is the underlying biochemical mechanism?

    Skip this one if you’re biochemically challenged…

    5-oxoproline (aka pyroglutamic acid) is produced from γ-glutamyl cysteine by the enzyme γ-glutamyl cyclotransferase. This enzyme’s activity increases when glutathione levels are low, due to a loss of feedback inhibition from glutathione.

    Thus the accumulation of pyroglutamic acid is thought to be due to depletion of the glutathione, particularly when glutathione synthetase is inhibited. Decreased activity of 5-oxoprolinase, which breaks down pyroglutamic acid, may also play a role.

    Check out the γ-glutamyl cycle to see how this all links up:

    GGcycle Metabolic Muddle #004

    Key: A = excess γ-glutamyl cysteine becomes a substrate for γ-glutamyl cyclotransferase, P = paracetamol, S = sepsis, F = flucloxacillin. From Dempsey et al, 2000. See also Q5.

    Simple, eh.

    —

    Q5. What factors may contribute to this?

    Factors that may contribute to pyroglutamic acidemia include:

    Drugs

    • paracetamol — depletion of glutathione by its metabolite N-acetyl-p-benzoquinoneimine (aka NAPQI)
    • flucloxacillin — inhibition of 5-oxoprolinase
    • vigabatrin

    Severe sepsis — depletion of hepatic glutathione pools due to oxidative stress from stimulated leukocytes, reperfusion of ischemic tissue, or endotoxemia

    Organ dysfunction — hepatic, renal

    Other — malnutrition, pregnancy

    Congenital enzyme deficiencies — e.g. glutathione synthetase deficiency (mental retardation, hemolytic anemia and metabolic acidosis)

    —

    Q6. What is the appropriate management?

    Management options include:

    • Stop or change exacerbating medications
    • Treatment or removal of source of sepsis (e.g. plam removal of hip prosthesis in this case)
    • Provide appropriate ICU-level management of severe sepsis and organ support —  intubation and ventilation as required, hemofiltration for renal failure, etc.
    • N-acetylcysteine — may help replenish glutathione stores.
    • Sodium bicarbonate — may not be beneficial in severe HAGMA.

    —

    References

    ResearchBlogging.org

    • Dempsey GA, Lyall HJ, Corke CF, & Scheinkestel CD (2000). Pyroglutamic acidemia: a cause of high anion gap metabolic acidosis. Critical care medicine, 28 (6), 1803-7 PMID: 10890623
    • Mizock BA, & Mecher C (2000). Pyroglutamic acid and high anion gap: looking through the keyhole? Critical care medicine, 28 (6), 2140-1 PMID: 10890683
    • Peter JV, Rogers N, Murty S, Gerace R, Mackay R, & Peake SL (2006). An unusual cause of severe metabolic acidosis. The Medical journal of Australia, 185 (4), 223-5 PMID: 16922670
    Filed Under Blood Results, Clinical Case, Intensive Care, Investigation [tests] Tagged With HAGMA, metabolic acidosis, pyroglutamic acid

    Choosing Life or Death

    January 30, 2010 By Chris Nickson 6 Comments

    Everyone who works in ED or ICU should read Alicia von Stamwitz’s brief but moving account of her father’s last visit to the emergency department:

    …

    The doctor explains what I already know: my father’s heart is weak, his kidneys are failing and his lungs are filling with fluid. For the second time in six months, he needs to have a tube inserted in his windpipe.

    I nod, waiting for him to continue listing procedures and tests. Instead, he takes a small step back from the gurney and asks, “Does your father have a living will?”

    I freeze. No emergency room doctor has asked me this before. I answer, evenly, yes. “Do you have durable power of attorney?” Yes.

    Visibly relieved, he looks me in the eye and gently but pointedly asks: “Does your father want us to employ extreme measures” — he pauses one heartbeat for emphasis — “knowing that he is not likely to improve?”

    …

    Read on here.

    Being compelled to make a life-or-death decision for a loved one is a nightmare scenario for anyone. As health professionals we may not always agree with the decision of a patient or his or her family – but sometimes it is their decision to make.

    It is our job to help and support them regardless.

    [Hat tip to Dr. Bearemy's My Emergency Blog]

    Filed Under Emergency Medicine, Intensive Care, Patients Tagged With Death, emergency, end of life, Intensive Care, life, patient

    Pulmonary Puzzle #008

    January 26, 2010 By Paul Young 4 Comments

    A 3o year old male presents with a 3 day history of fevers and increasing breathlessness.  On presentation he is noted to be severely hypoxic with sats of 80% on room air.  The following chest X-ray is obtained:

    image 17 Pulmonary Puzzle #008Questions

    Q1. Describe the chest X-ray and outline the differential diagnosis

    There are diffuse bilateral pulmonary infiltrates which have a nodular appearance. The differential diagnosis here includes infectious causes such as viral pneumonia and typical and atypical causes of bacterial pneumonia. Non-infectious causes would include hypersensivity pneumonitis and diffuse alveolar haemorrhage. The short history favours an infectious aetiology.

    —

    The patient is admitted to the intensive care unit and continues to deteriorate with an increasing oxygen requirement. An arterial blood gas shows a PaO2 of 55 on 15L O2 via a facemask. The respiratory rate rises to the high 40s. Another chest X-ray is obtained:

    image 26 Pulmonary Puzzle #008Q2. Describe the chest X-ray now. What would you do next? What problems would you anticipate?

    The chest X-ray shows worsening of the previous alveolar infiltrates. The combination of the early rapid progression in the clinical and radiological course combined with the severity of the hypoxia indicates that intubation is required. Non invasive ventilation is not a good option here (except while preparing to intubate) as delaying intubation further here is only likely to make the procedure more dangerous by further limiting the patient’s reserve. The problem that you need to need to anticipate here is rapid desaturation and potential difficulty obtaining adequate oxygenation with bag-mask ventilation if that occurs

    —

    Over the following 12 hours the patients condition continues to worsen to the point that the patient is frequently desaturating on 100% oxygen with a PEEP of 18. You are asked to see the patient because the patient has desaturated to 80% on the above settings. The ventilator appears to be working appropriately. On examination, you find the right chest is moving less than the left and there is less air entry on that side.

    Q3. What do you do now?

    Order a chest X-ray. Even if you are very strongly suspicious that there is a pneumothorax you should not perform needle decompression here. It is likely given the clinical context that the change here represents progression of disease. If there is no pneumothorax and you create one there is a significant risk that the patient will die.   In this case, there was no pneumothorax:

    image 3 Pulmonary Puzzle #008

    —

    Q4. What are the options for improving oxygenation now?

    This patient is failing conventional ventilation. The options for improving oxygenation are:

    1. nitric oxide

    2. prone ventilation

    3. inverse ratio ventilation

    4. ECMO

    5. High Frequency Jet Ventilation

    —

    A non-conventional ventilation strategy is employed and the following chest X-ray is obtained:

    image 4 Pulmonary Puzzle #008

    Q5. Describe the chest X-ray.

    This x-ray shows an ECMO cannula inserted via the right internal jugular route. With this particular cannula, venous blood is taken from the superior vena cava and the inferior vena cava. It is then oxygenated and the cannula has a third lumen which allows arterialised blood to be directed towards the tricuspid valve in the right atrium under TOE guidance.

    —

    On ECMO things got worse…

    image 18 Pulmonary Puzzle #008

    and then they got better…
    image 6 Pulmonary Puzzle #008

    Q6. Describe the most recent chest x-ray.

    The chest x-ray has dramatically improved. However, there is a small right basal pneumothorax.

    —

    Filed Under Chest X-Ray, Clinical Case, Intensive Care, Investigation [tests], Medical Specialty, Respiratory Tagged With ECMO, high frequency jet ventilation, nitric oxide, pneumonia, refractory hypoxaemia

    Pulmonary Puzzle #007

    January 12, 2010 By Paul Young 12 Comments

    A 67 year old gentleman with a BMI of 45 was waiting for his respiratory outpatient clinic appointment.  While waiting, he fell asleep.  A medical emergency was called because he could not be woken up.  On arrival of the MET team the patient is found to have a blood pressure of 140/70, a heart rate of 100bpm and oxygen sats of 68% on room air.  He is breathing spontaneously but requires airway support.  His  GCS is 3/15.  Supplemental oxygen is applied and the following arterial blood gas is obtained.

    image 1 Pulmonary Puzzle #007

    Questions

    Q1. Describe the arterial blood gas?

    There is a moderately severe acidaemia due to severe respiratory acidosis. There is a marked metabolic alkalosis which indicates that there is likely to be severe underlying hypercapnic respiratory failure. The oxygen saturation is 97%.

    Q2. If the baseline bicarbonate is 46, what is the baseline CO2?

    In a chronic respiratory acidosis the bicarb rises by 4 for every 10mmHg rise in the CO2. So, a bicarb of 20 above normal corresponds to a CO2 of 50 above normal. In other words, the baseline CO2 would be about 90mmHg!

    Q3. Is supplemental oxygen a good idea in this case?

    Yes. Without supplemental oxygen, a CO2 of 132mmHg is not compatable with life. Calculating the PAO2 from the alveolar gas equation for a patient on room air demonstrates this:

    image 2 Pulmonary Puzzle #007
    While supplemental oxygen may precipitate worsening type 2 respiratory failure in patients with chronic hypercapnia, removing supplemental oxygen in the setting of such extreme hypercapnia will precipitate death.

    Filed Under Blood Results, Intensive Care, Investigation [tests], Respiratory Tagged With arterial blood gases, clinical cases, type 2 respiratory failure

    Don’t put your Patient in a Box

    January 7, 2010 By Chris Nickson 15 Comments

    The fourth rule of Expensive Scare Medicine is:

    “If you measure something and it is not normal,
    make it normal,
    if it is safe to do so.”

    Rule 4 is a tried-and-tested heuristic for looking after critically ill patients – it is useful so long as the last seven words are remembered with due emphasis.

    ‘Euboxia‘ is the pathophysiological state whereby ‘all boxes on a pathology print-out are in the normal range’ (Reade, 2009). Many people working in critical care settings experience an insatiable desire to achieve this state for their patients. Unfortunately finding a blood test abnormality does not mean that correcting it will make the patient better.

    An example I came across recently concerns the ‘common knowledge’ (in other words, there is no convincing evidence that it is true) that having more than two relatives at the bedside of an ICU patient is a poor prognostic indicator (Reade, 2009). Unfortunately for euboxophiles, asking relatives to leave does not help the situation! The converse also appears to be true. A paucity of relatives relative to the severity of illness is suggestive of a bad outcome. Reade has termed this ‘relative relative insufficiency’, and correcting it by dragging relatives to the bedside doesn’t seem to be beneficial. Bearing this in mind, I’ll leave to you to decide if corticosteroid treatment is an efficacious therapy for ‘relative adrenal insufficiency’ in septic shock…

    Indeed, euboxia may not just be unhelpful, sometimes it can put your patient in a box  – a coffin-shaped box. Here are some examples of when the quest for euboxia can lead to nothing but trouble:

    • lung protection strategies aimed at preventing ventilator-associated lung injury in acute respiratory distress syndrome (ARDS) don’t work if you try to correct the PaCO2 – permissive hypercapnia and moderate acidosis (e.g. pH >7.1) are acceptable and often necessary.
      [See Pulmonary Puzzle #006 Q4]
    • Allowing PaCO2 to normalise after intubating a patient with severe metabolic acidosis can be fatal. Patients with severe illnesses like diabetic ketoacidosis or septic shock hyperventilate (resulting in hypocapnia) to compensate for their underlying metabolic acidosis. This has to be maintained when they are started on mechanical ventilation.
      [See EMCrit Podcast 3 - Intubating the patient with Severe Metabolic Acidosis]
    • Toxicologists often find themselves embracing abnormality. Systemic alkalinsation with sodium bicarbonate or hyperventilation of the intubated patient (to pH 7.5-7.55) is a mainstay of the management of severe tricyclic antidepressant overdose.
      [See Toxicology Conundrum #022]
      ‘Dysboxia’ is also useful in the setting of salicylate overdose. Urinary alkalinsation with sodium bicarbonate increases the renal clearance of aspirin, and again, when intubated, hyperventilation should be maintained to prevent catastrophic effects from uncovering a decompensated metabolic acidosis.
    • Over-enthusiastic correction of abnormalities that ’should’ be ‘normal’ may cause harm. The patient with chronic hyponatremia runs the risk of central pontine myelinolysis if they are aggressively treated with hypertonic saline.
      [See NEJM Clinical Image - Central Pontine Myelinolysis]
      Similarly, excessive correction of hypertension, particularly in the patient who has just had a stroke, may result in cerebral hypoperfusion if the patient can no longer autoregulate blood flow at ‘normal’ blood pressures.
    • In patients with penetrating trauma, excessive fluid resuscitation should generally be avoided. It may be better to aim for a ‘low-to-normal’ blood pressure (e.g. MAP 65 mmHg) that is adequate for organ perfusion and reduces the risk of further catastrophic hemorrhage prior to operative intervention.
      [See EMCrit Podcast 12 - Trauma Resus: Part I]
    • In most critically ill patients with anaemia, transfusing significantly above a hemoglobin of 70 g/L does not seem to improve outcomes, and may lead to transfusion-related complications.
    • Over-oxygenation of the patient with chronic obstructive pulmonary disease (COPD) reliant on hypoxemic drive is an oft-cited pitfall in critical care. Aiming for a ‘normal’ oxygen saturation can be harmful in other settings as well. Oxygen therapy for paraquat toxicity, or the oncology patient treated with bleomycin, may actually increase the free radical damage caused by reactive oxygen species (ROS) and contribute to severe pulmonary fibrosis. Aiming for oxygen delivery sufficient for, but not in excess of, organ requirements may be beneficial – even with sub-normal oxygen saturations (e.g. SaO2 in the high 80s).
      [see Oncology Quandary #003 Q4]

    Indeed, ‘normality’ is an elusive concept. ‘Normal’ people can have values that lie outside of the ‘normal’ range (for instance, if the reference interval is +/- 2 standard deviations from the mean ‘only’ 95% of the ‘normal’ population will fall within this range). Being outside of the ‘normal’ range might simply mean that, yes, you are part of a bell curve and that, yes, we humans are a diverse lot – it doesn’t necessarily mean you are sick. Furthermore, ‘normal’ values can lead us astray. A patient with a ‘normal’ creatinine can still have acute kidney injury. A patient with a ‘normal’ white count and C-reactive protein (CRP) can still have septic shock or osteomyelitis. And finally, it is often difficult know exactly what ‘normal’ is – normality is sometimes simply a matter of convention and tradition. After all, what exactly is health? What exactly is disease?

    “Conventions and traditions, I suppose, work blindly but surely for the preservation of the normal type…”
    -Ford Maddox Ford, from The Good Soldier.

    Being guided by laboratory tests in preference to clinical judgment is a fool’s game. A game we can avoid playing by striving to truly understand the pathophysiology underlying our patients’ illnesses. Instead of looking at a patient and his or her illness as an impenetrable ‘black box’ we can think about what is happening inside the box and why. In doing so we may better help our patients, even when the evidence is contradictory or when the clinical picture is muddled.

    Facts alone will not be of much service to you unless studied in connection with others and with the phenomena displayed during life.
    - William Osler

    If you have a good example of when ‘euboxia goes bad’ leave a comment!

    ResearchBlogging.org
    Reade MC (2009). Should we question if something works just because we don’t know how it works? Critical Care and Resuscitation, 11 (4), 235-6 PMID: 20001869


    This post is featured in Grand Rounds Volume 6, Number 16 hosted by the Covert Rationing Blog.

    Filed Under Emergency Medicine, Featured, Intensive Care, Investigation [tests], Toxicology Tagged With critical care, euboxia, heuristic, Investigation [tests], normal, pathophysiology, test

    Oncology Quandary #003

    January 6, 2010 By Chris Nickson 10 Comments

    A 26 year-old male, with no previous history of seizures, was BIBA in status epilepticus. He was intubated for seizure management with propofol and clonazepam infusions.

    A chest XR was performed:

    MET TEST LUNG CXR Oncology Quandary #003

    Chest radiograph

    Q1. What does the chest radiograph show and what is the likely diagnosis?

    The chest radiograph shows ‘cannon ball’ lesions – multiple bilateral spherical lesions of varying size that are predominantly preipherally located.
    An endotracheal tube and nasogastric tube are present and appropriately positioned.

    The likely diagnosis is metastatic cancer involving the lungs.

    But where is the primary?

    • Tumors with rich systemic venous drainage are most likely to metastasize to the lungs.
      e.g. choriocarcinomas, melanomas, testicular germ cell tumours, renal cancers, osteosarcomas and thyroid carcinomas.
    • However, lung metastases most commonly arise from more common tumours.
      e.g. breast, colorectal, prostate, bronchial, head/neck, and renal cancers.

    Q2. What should be specifically looked for on clinical examination?

    The following should be carefully examined in a patient with suspected malignancy:

    • all lymph nodes draining the region of a suspected lesion
    • all remaining accessible lymph node groups
    • the abdomen, specifically looking for hepato/splenomegaly and ascites
    • the testes
    • rectum
    • lungs
    • breasts and pelvis in females
    • skin, nails and retina for melanoma
    • focal neurological deficits

    A large right-sided firm scrotal mass was palpable on physical examination and an urgent urology referral was made.

    Ultrasonography confirmed the mass to be intratesticular with normal surrounding tissues. The mass was solid, ~6 cm in diameter, and had some cystic changes and slightly increased vascularity.

    MET TEST USSnorm Oncology Quandary #003

    Sagittal view of normal testis

    MET TEST USSabnorm Oncology Quandary #003

    Sagittal view of abnormal testis

    A CT head and chest were also performed, followed by an MRI of the brain, abdomen and pelvis once the patient was extubated. Sample images from the CT chest and MRI brain demonstrating the presence of lung and cerebral metastases are shown below:

    MET TEST LUNG CTchest Oncology Quandary #003

    CT Chest

    MET TEST LUNG MRIbrain Oncology Quandary #003

    MRI brain

    Q3. Based on the findings in Q3 what is the likely diagnosis? What are the different types?

    Metastatic testicular cancer.

    • Testicular cancer is the most commonly diagnosed cancer in men between the ages of 15 years and 35 years.
    • About 1 in 20 testicular cancers have already metastasised at the time of diagnosis, and a similar number involve both testes.
    • Risk factors include:
      cryptorchidism, family history (especially first degree relatives), genetic disorders (e.g. Klinefelters and Down syndrome), infertility, testicular atrophy, HIV, white race and smoking.

    There are numerous different types of testicular cancer. 95% are germ cell tumours (GCTs) and 1 in 3 of these are mixed cell types. Of the pure GCTs the main distinction is between:

    • seminomas (~50%)
    • non-seminoma germ cell tumours (NSGCT):
      • including embryonal carcinomas, yolk sac tumours, teratomas, and choriocarcinomas
      • mixed cell type tumours behave like NSGCTs.
      • These are more aggressive than seminomas.

    This patient was diagnosed with a NSGCT as both beta-human chorionic gonadotrophin (bHCG) (>350,000 mIU/mL) and alpha-fetoprotein (AFP) were grossly elevated.

    • AFP is not elevated in pure seminomas.

    The patient underwent a unilateral orchidectomy and BEP chemotherapy (bleomycin, etoposide and cisplatin) was commenced. He may also need radiotherapy and/or surgery to treat his cerebral metastases.

    Q4.  What toxicities due to the chemotherapy (mentioned in the answer to Q3) may occur?

    The major immediate toxicities associated with administration of BEP chemotherapy are:

    • fatigue (39%)
    • mucositis (25%)
    • sensory neuropathy (20%)
    • acute pulmonary toxicity (13%)
    • ototoxicity (10%)
    • hematologic toxicity (9%)

    The components of BEP have different mechanisms of action and have different treatment toxicities:

    • Bleomycin
    • Inhibits DNA and to a lesser extent RNA synthesis, produces single and double strand breaks in DNA possibly by free radical formation.
      Toxicities:

      • Pneumonitis that may lead to pulmonary fibrosis and death. Onset may be delayed up to 6 months. Risk is increased by use of supplemental oxygen, so minimal oxygen flow should be administered to maintain SaO2 ~88-92%.
      • Chest pain and fever may be associated with administration. Myelosuppression is generally mild. Gastrointestinal symptoms, rashes and mucositis may occur.
    • Etoposide
      A podophyllotoxin that inhibits topoisomerase II resulting in DNA strand breaks and inhibition of cell division in the late S and G2 phases of the cell cycle.
      Toxicities:

      • myelosuppression, neuropathy, gastrointestinal symptoms, and rashes – including Stevens-Johnson syndrome.
    • Cisplatin
      A platinum-based compound that is activated within the cell by displacement of chloride ions, leaving positively charged molecules which react with DNA. DNA replication, transcription and cell division are inhibited, ultimately inducing apoptosis. It is cell cycle nonspecific and other mechanisms may also be involved.
      Toxicities:

      • Cardiovascular effects (delayed): hypertension, dyslipidemia, coronary artery disease, thromboembolic events and Raynaud phenomenon.
      • Neuropathy, seizures and ototoxicity.
      • Nephrotoxicity as well as hypomagnesemia, hypophosphatemia and hypokalemia.
      • Myeolosuppression, gastrointestinal symptoms and rashes.

    Secondary malignancies are the most common cause of death in testicular cancer survivors (leukemia and solid tumours) and infertility is common.

    Q. What is this patient’s prognosis?

    Testicular cancer has 95% survival overall and about 80% survival in the presence of metastases.

    However, this patient falls into the category of “poor-prognosis NSGCT” given that his bHCG is >50,000 mIU/mL. His 5 year survival is probably <70%.

    References

    • Australian Medicines Handbook
    • Emedicine
    • Kaufman DS, Saksena MA, Young RH, Tabatabaei S. Case records of the Massachusetts General Hospital. Case 6-2007. A 28-year-old man with a mass in the testis. N Engl J Med. 2007 Feb 22;356(8):842-9. PMID:  17314344
    • Kaufman MR. Short- and long-term complications of therapy for testicular cancer. Urol Clin North Am. 2007; 34(2): 259-68. PMID: 17484931
    • Shaw J. Diagnosis and treatment of testicular cancer. Am Fam Physician. 2008; 77(4): 469-74. PMID: 18326165
    Filed Under Chest X-Ray, Clinical Case, Intensive Care, Oncology Tagged With brain, chemotherapy, lung, metastasis, seizure, testicular cancer

    Swine Flu Saves Lives?

    January 5, 2010 By Chris Nickson 8 Comments

    I read Richard Lehman’s roundup of the major medical journals nearly every week on doc2doc. He provides the perspective of a wise yet whimsical generalist who’s been ‘around a while’. One of the papers he reviewed in his January 4th edition was the recently published overview of the Australian swine flu pandemic:

    • Bishop JF, Murnane MP, & Owen R (2009). Australia’s winter with the 2009 pandemic influenza A (H1N1) virus. The New England Journal of Medicine, 361 (27), 2591-4 PMID: 19940287 (fulltext)

    Lehman’s perspective on this was:

    Tucked away in a commentary article about the Australian H1N1 influenza pandemic is the most startling observation:

    A broader measure of all Australian deaths resulting from influenza or pneumonia currently indicates that there have been fewer such deaths than in other influenza or winter seasons.

    Someone in the BMJ Rapid Responses had already seen these Antipodean figures some weeks ago and made the deduction that H1N1 saves lives. The pandemic strain seems to be displacing seasonal flu variants with higher overall lethality. We should be giving H1N1 a warm welcome, if only it didn’t kill young people preferentially.

    The last sentence is the kicker really – it hints at the swine flu paradox – decreased mortality coupled to higher-than-expected impact on critical care services. Bishop et al summarize the Australian ICU experience thus:

    A distinguishing feature of the epidemic was the number of people who were hospitalized in ICUs with confirmed cases of pandemic H1N1 influenza (3.5 per 100,000) and their young age (median, 42 years). According to data from influenza reports and from the Australian government, a total of 387 adults (over 20 years of age) were admitted with viral pneumonitis resulting from influenza A, as compared with a median of only 57 adults per year admitted with viral pneumonitis from any cause between 2005 and 2008. The peak of the epidemic in Australia lasted about 3 weeks, and although the Australian health system was stressed, there was spare capacity of ECMO equipment, hospital beds, and ICU beds.

    It is because swine flu has ‘two faces’ that I do not welcome the 2009 H1N1 virus as a respite from its more lethal seasonal cousins. As it is the young that swine flu targets, even though fewer indivduals may die, more life-years may be lost and at greater cost. That is why I had my swine flu vaccine, even though I don’t have the numbers to prove it.

    ECMO chest Swine Flu Saves Lives?

    Swine flu saves lives? Not according to this chest radiograph…

    Swine Flu Links and References

    Filed Under Infectious Disease, Intensive Care Tagged With doc2doc, ICU, mortality, pandemic, richard lehman, swine flu

    Pulmonary Puzzle #006

    January 4, 2010 By Chris Nickson 17 Comments

    A 36 year-old immunosuppressed male was infected with swine-origin influenza virus (SOIV, the 2009 H1N1 pandemic influenza A virus). He had required 3 weeks of mechanical ventilation for ‘FLAAARDS’ (‘flu’ A-associated acute respiratory distress syndrome) resulting in type 1 and 2 respiratory failure, which was complicated by bilateral pneumothoraces. These were treated with bilateral intercostal catheters (ICCs). Overnight the inspiratory pressures needed to maintain his tidal volume had progressively increased and his face had become markedly swollen.

    A chest radiograph was performed:

    subcut emphysema1 Pulmonary Puzzle #006

    Chest radiograph 1

    Q1. Describe the chest radiograph.

    Chest radiograph findings:

    • supine film.
    • tracheostomy tube, right internal jugular central venous catheter, and a nasogastric tube are all visible and appropriately positioned.
    • bilateral infiltrates consistent with ARDS.
    • bilateral ICCs are present (somewhat kinked on the left), as well as two pigtail ‘pneumocath’ tubes on the right side.
    • although there is no pneumothoraces visible on this supine film there is widespread severe subcutaneous emphysema. The subcutaneous emphysema extends up the neck and along both upper limbs. There is also a rim of air below the diaphragm, particularly between the left hemidiaphragm and the stomach.

    Subcutaneous emphysema is usually the result of a pneumothorax, but can also result from surgical procedures (such as gas insufflation during laparoscopy), esophageal rupture or a pneumomediastinum.

    Q2. What findings would you expect on clinical examination?

    Findings may include:

    • Diffuse swelling of the involved regions:
      • usually the chest and neck, but extending to the head, upper limbs and abdomen in this case.
    • On palpation there may be a crackling sensation (may be absent if the subcutaneous gas is trapped locally).
    • Breath sounds will be diminished.
    • There may also be evidence of ‘tensioning‘:
      • cyanosis due to hypoxemia, decreased chest wall movement with ventilation, neck vein distention, tachycardia and hypotension. Unchecked, this results in death.

    Q3. What immediate management is indicated?

    Pneumothoraces can usually be treated with 14-20 French gauge ICCs, often using a Seldinger technique. However, in this case, bilateral large bore ICCs were inserted as the air leak is already exceeded the capacity of multiple tubes.

    As marked pneumothoraces are not visible, air may be leaking around the tubes at the sites of ICC insertion. An attempt at sealing these sites with sutures and occlusive dressings is appropriate. However, it is not possible to close the pleural lining so these measures may not prevent the ongoing egress of air subcutaneously.

    A repeat chest radiograph taken two days after the above treatment measures is shown:

    subcut emphysema3 Pulmonary Puzzle #006

    Chest radiograph 2

    Q4. What measures may help prevent a recurrence?

    Avoid barotrauma.

    • Use a mechanical ventilation strategy that maintains adequate oxygenation (e.g. PaO2 >55 mmHg) and avoids excessive acidemia (e.g. keep pH >7.1) but allows permissive hypercapnia (with a tidal volume of 6-8 mL/kg) and minimises barotrauma (aim for plateau pressures <30 cmH2O).
    • In refractory cases high frequency oscillatory ventilation (HFOV) or extracorporeal membrane oxygenation (ECMO) may be considered.

    Ensure adequate insertion and functioning of ICCs.

    • avoid making an excessive hole on ICC insertion (should be large enough to admit a finger). [SEE COMMENTS]
    • ensure all ICC side port openings are within the pleural space.
    • rotate the ICC through 360 degrees after insertion to decrease the risk of tube kinking.
    • try to obtain an adequate seal around the ICC insertion sites: close the wounds with sutures, seal with petroleum gauze and apply an occlusive dressing. [SEE COMMENTS]
    • persistent air leaks may require the insertion of multiple ICCs (e.g. bronchopleural fistulae).
    • apply suction initially (e.g. -20 cmH20 at the wall) – but remember that the amount of suction in the ICC is dependent on the depth of water in the water seal reservoir, not on the suction from the wall valve.
    • monitor chest drains to ensure they are still bubbling or ’swinging’.

    Monitor closely for evidence of pneumothorax and subcutaneous emphysema.

    Refractory air leaks may require surgical intervention:

    • this is usually considered after  72 hours of persisting air leak or if lung re-expansion has not occurred.
    • Options range from bronchoscopic repair using sealing agents (e.g., fibrin glue, albumin-glutaraldehyde tissue adhesive, stents, metallic coils, bone, absolute alcohol, Nd:YAG laser) to thoracostomy and lobectomy.

    Filed Under Clinical Case, Intensive Care, Radiology, Respiratory Tagged With chest drain, chest radiograph, immunosuppression, influenza, intercostal catheter, mechanical ventilation, subcutaneous emphysema, swine

    Bad News Broken

    January 1, 2010 By Chris Nickson 13 Comments

    The patient’s son and two daughters had said little during the family meeting. The older daughter steadied her sister’s trembling hand while the son stared at the doctor intently.

    The doctor felt that he may have said too much, that he may have clouded his message. He decided to sum up the situation, “I’m very sorry but your father’s heart is just too weak. Although we are doing everything we can to help him, I think he is going to die.”

    The doctor stopped speaking and turned to the nurse beside him who nodded sadly. He looked at each of the patient’s children, trying to give them enough time to comprehend how negligible their father’s chance of recovery was. He saw mascara and teardrops mix and merge into murky streaks on the women’s cheeks.

    Finally the doctor asked, “Do you have any questions for me?”.

    The patient’s son stretched his arms above his head and with interlocked fingers cracked his knuckles. He said, “Doc, can you tell me where the cafeteria is? I could murder a burger…”

    murder burger Bad News Broken

    The now infamous recruitment ad for a NZ burger bar.

    Filed Under Intensive Care, Literary Medicine, Patients Tagged With bad news, Death, family, grief, patient

    Cardiovascular Curveball #003

    December 27, 2009 By Chris Nickson 6 Comments

    As leader of the MET team you were called to a ‘Code Blue’ to resuscitate a 57 year-old man who arrested on the ward post-operatively. The initial rhythm was ventricular fibrillation. Following defibrillation (1 x 200J biphasic), 1 mg adrenaline IV and 2 minutes of CPR he had an idioventricular rhythm with a rate of 40 but remained pulseless. CPR was continued for a further 2 minutes and 1.2 mg atropine was administered. The patient then had return of spontaneous circulation and was intubated as he remained unconscious.

    This was his ECG post-intubation:

    RonT 31 Cardiovascular Curveball #003

    Post-resuscitation ECG (click to enlarge)

    Q1. Describe this ECG.

    This is an unusual ECG!

    • There is an underlying sinus rhythm with normal axis.
    • The QRS complexes are high voltage with markedly prolonged QT intervals (although the ends of many of the T waves are not easily seen).
    • There is a broad complex (~120 msec) QRS occurring on every second T wave… This is consistent with bigeminal ventricular premature contractions (VPBs) with recurrent R-on-T phenomenon.

    Q2. Can you guess what happened next?

    He arrested again – this time the ECG monitor was suggestive of torsades de pointes (‘twisting of the points’) – presumably because of the barn-door R-on-T phenomenon seen in the above ECG.

    He reverted to sinus rhythm following 1 x 200J biphasic defibrillation. However, the ECG monitor showed that he soon returned to the rhythm shown in his post-intubation ECG.

    He was not in torsades de pointes long enough to capture a 12-lead ECG – but this is what it looks like:

    Hypokalemia leading to Torsades des Pointes

    An R-on-T phenomenon leading to Torsades des Pointes (click to enlarge)

    The features of torsades de pointes are:

    • polymorphic ventricular tachycardia with a rate of >200/min.
    • The axes of the QRS complexes undulate with the polarity of the complexes appearing to shift about the baseline.
    • often occurs in short episodes (<90 seconds) but prolonged episodes can occur.

    —-

    His arterial blood gas post-intubation showed:

    pH 7.403 [7.350 - 7.450]
    pCO2 48.6 mmHg [36.0 - 45.0]
    pO2 176 mmHg [85.0 - 110]
    Bicarbonate 29.7 mmol/L [21.0 - 28.0]
    Sodium 130 mmol/L [134 - 146]
    Potassium 2.6 mmol/L [3.4 - 5.0]
    Chloride 98 mmol/L [98- 108]
    Glucose 8.6 mmol/L [3.0 - 5.4]
    Lactate 1.8 mmol/L [<1.3 mmol/L]

    Q3. Describe the arterial blood gas.

    The patient is ‘over-oxygenated’. pH is normal with a mild respiratory acidosis and mild metabolic alkalosis. There is mild hyponatremia, hyperglycemia and a mild hyperlactemia.

    Overall this is a great gas for someone who just had a cardiac arrest!

    The key abnormality though is the presence of hypokalemia, which is likely to have a causative role in this patient’s predilection for torsades.

    Q4. What further management is necessary?

    Correction of moderate hypokalemia (1.5 – 3.5 mmol/L) with potassium and administration of magnesium for impending torsades de pointes.

    The patient was administered 20 mmol of KCl IV over 5 minutes via a central line and was administered 10 mmol MgCl2 IV.

    Following the further management given in Q4, the patient had another ECG:

    HOCM PostRx RonT21 Cardiovascular Curveball #003

    ECG following further management

    Q5. Describe the ECG findings. Is the ECG suggestive of an underlying diagnosis?

    The ECG findings are:

    • Rate and rhythm:
      Atrial fibrillation (irregularly irregular with absent P waves) with a heart rate of ~ 100/min.
    • Axis:
      Normal.
    • QRS complexes:
      The QRS complex meets voltage criteria for left ventricular hypertrophy:

      • Sokolow and Lyon criteria: S(V1) + R(V5 or V6) > 35 mm
      • Framingham criteria: S(V1 or V2) + R(V5 or V6) > 35 mm.
    • QT interval:
      prolonged (QTc ~500)
    • ST segments:
      ST depression (up to 2-3 mm) predominantly in anterolateral leads (I,II, aVL and V3-V6)
    • T waves:
      widespread biphasic T waves

    Review of this patient’s notes showed that a coronary angiogram 1 year previously has excluded coronary artery disease. However an echocardiogram was also perfomed at this time, the findings were consistent with severe hypertrophic obstructive cardiomyopathy (HOCM).

    Emergency and critical care doctors need to look for the classic features of HOCM on the ECGs of patients presenting with syncope or arrhythmias. The ECG is abnormal in about 90% of HOCM cases and features include:

    • non-specific findings such as increased QRS voltage, QRS widening, ST segment and T waves changes consistent with hypertrophy.
    • deep narrow Q waves in the lateral leads (I, II, aVL, V5, V6) with high voltage QRS’s in a younger patient with syncope is considered a specific finding highly suggestive of HOCM (not present in this patient’s ECG).

    Check out the free ‘EMRAPTV episode 65: Syncope‘ to hear Amal Mattu discussing the “not-to-miss” ECG findings in the patient presenting with syncope.

    Q6. What does ST elevation in aVR mean?

    Never forget to scrutinize aVR for ST elevation (STE) in a patient who may be having an acute coronary syndrome:

    It is 95% specific for left main coronary artery (LMCA) occlusion when there is evidence of ischemia in other leads (typically widespread ST depression).

    Patients with significant STE in aVR due to an acute coronary syndrome have a 70% chance of developing cardiogenic shock or dying – and medical treatment (including thrombolysis) does nothing to change this… They need to go to the cath lab STAT!

    The post-treatment ECG shown above has features consistent with an LMCA occlusion, however:

    • the patient had atrial fibrillation and structural heart disease (HOCM) which may account for the ECG findings.
    • the patient had a recent ‘normal’ coronary angiogram and an ECG at that time (although sinus rhythm was present) had a similar pattern of ST segment changes.

    Finally, here are some more scary things to know about acute coronary syndromes with ST elevation in aVR (these do not apply in the absence of evidence of ischemia in other leads, nor in the presence of supraventricular tachycardias):

    • STE in aVR and aVL is highly specific for LMCA stenosis.
    • STE in aVR and V1 is specific for proximal left anterior descending (LAD) or LMCA stenosis. If the STE in aVR is greater than the STE in V1 this indicates LMCA stenosis (81% sensitivity, 80% specificity, and 81% accuracy) rather than LAD.
    • STE in aVR >1.5mm has ~75% mortality!

    References

    • Williamson K, Mattu A, Plautz CU, et al. Electrocardiographic applications of lead aVR. Am J Emerg Med 2006;24:864-874. PMID: 17098112.
    Filed Under Cardiology, Clinical Case, ECG, Emergency Medicine, Intensive Care Tagged With cardiac arrest, HOCM, hypertrophic obstructive cardiomyopathy, hypokalemia, torsades de pointes

    Down with the Afterload!

    December 10, 2009 By Chris Nickson 11 Comments

    “Is this the intensive care unit?” asked Alice in a reverent whisper.

    “It says so doesn’t it,” said Dr. Rabbit pointing to the writing on the glass doors which said “TINU ERAC EVISNETNI” backwards though because they were now inside the unit looking out.

    “These patients are the sickest you ever saw. These doctors are the smartest in the world. These nurses know more than the doctors; well, they know a lot more than I do. Here technology triumphs over disease. Facts, not guesses. Nouns are better than adjectives. Numbers are the best kind of nouns. Here we can measure everything. With measurements we can do calculations. With calculations we can do logarithms. With logarithms we can solve any clinical problem.”

    If you are new to intensiveland and find yourself bamboozled by all the numbers, indices and machines that go ping. There is only one reference you need turn to:

    Bartlett RH. Alice in intensiveland. Being an essay on nonsense and common sense in the ICU, after the manner of Lewis Carroll. Chest. 1995 Oct;108(4):1129-39. PMID: 7555127 (fulltext pdf)

    Using this paper you can learn the art of presenting an ICU patient to your peers:

    Alice was very impressed by this scholarly presentation. It seemed to her that Dr. Rabbit had explained what was wrong with Mr. Hatter by describing all the things which he did not have. She thought how very difficult it must be, no, she thought how it was not easy, to develop this unusual method of syntax. Everyone on rounds seemed quite content, no, not uncontented with the presentation.

    You will finally understand the relationship between oxygen delivery and the production of reactive oxygen species thanks to Dr Dumpty’s editorial titled ‘Jabberwoxy’. Its starts as follows:

    Twas septic and the slimy rods
    Did gyre and gimble in the blood.
    All mimsy were the neutrophobs
    More air to fuel the flaming flood.

    You will learn to master ventilation from Dr. Knight:

    “I’ve been practicing and practicing with mechanical ventilators to try to make the blood gases normal. It’s not too hard if you just use enough pressure and enough oxygen.”

    “I do believe you are getting the hang of it Knight,” said Dr. Queen. “What’s that plastic tube sticking into his side?”

    “He had a pneumothorax a few days ago, so we put in a chest tube. I didn’t mention that we had to turn the tidal volume to 900 mL to get our 700 mL exhaled tidal volume.”

    And you will be able to make up your own mind about whether or not Dr. Queen is correct when he exclaims:

    “Down with the Afterload!”

    AlicebyRobinson2 Down with the Afterload!

    Filed Under Intensive Care, Medical Humor, Uncategorized Tagged With alice in wonderland, humour, huomour, Intensive Care

    Top 10 Rules of Expensive Scare Medicine

    December 10, 2009 By Paul Young 5 Comments
    1. Coagulopathy does not cause you to bleed precipitously from a single drain; this is an indication for a re-inspection of surgical excellence.
    2. A patient with a worsening metabolic acidosis after damage control laparotomy is usually still bleeding
    3. If you think that a patient who has had an abdominal aortic aneurysm repair might have dead gut then they do
    4. If you measure something and it is not normal, make it normal if it is safe to do so.
    5. Penicillin, flucloxacillin, cephazolin  and vancomycin is not a good combination for antibiotic prophylaxis even if the surgeon suggests it.
    6. If the surgeon says that a septic patient is too sick for an operation there are only two possibilities:
      1. the surgeon is wrong
      2. the patient is dead
    7. Usually if you ask an Oncologist how long a patient with a metastatic cancer who has exhausted all treatment options is going to live, they will tell you ‘one year’.  This is an ‘oncologist year’.  In order to work out the patient’s actual life expectancy, you should begin by halving the number of days in a year  (giving you a figure of approximately 182) and then you should subtract the patient’s age.  If the patient is currently admitted to the intensive care unit, you should subtract 10 for every organ system that has failed.   This figure will give you the patient’s life expectancy.  For patients outside the intensive care unit, this figure is in days.  For patients in the intensive care unit, this figure is in hours.
    8. If a patient who has had a bone marrow transplant is admitted to an intensive care unit they are in big trouble and when they engraft it does not mean they are getting better.
    9. Neurosurgeons like doing operations.  If a  patient achieves flexion this is a good outcome.
    10. Every patient you ever treat is going to die; if they are 85,  it is likely to be sometime soon.
    Filed Under Handy Hints, Intensive Care, Medical Humor, Top 10 Tagged With expensive scare medicine, ICU, intensive care medicine, Learning List, Top 10

    Pulmonary Puzzle #003

    November 30, 2009 By Paul Young 8 Comments

    Consider a 73 year-old female admitted with vomiting and subsequent chest pain.
    This is her erect AP admission chest X-ray.

    Pulmonary Puzzle #003

    Pulmonary Puzzle #003

    Questions

    Q1. Describe the chest X-ray?

    There is extensive mediastinal emphysema and bilateral pleural effusions.

    Q2. What is the diagnosis?

    Boerhaave syndrome or so-called ’spontaneous’ rupture of the oesophagus. Often it is not really spontaneous as it occurs with vomiting.

    Herman Boerhaave described the condition in 1724, in a classic example of clinicopathological correlation, when faced with the case of the Grand Admiral of the Dutch Fleet, a roast duck and three litres of juniper beer…

    Legend has it that letters Boerhaave received bore no address and were simply mailed “To the Greatest Physician in the World”.
    - from Tan SY, Hu M. Hermann Boerhaave (1668-1738): 18th century teacher extraordinaire. Singapore Med J. 2004 Jan;45(1):3-5. PMID: 14976574

    Q3. What is the classic presentation of this condition?

    “A middle-aged man presenting with sudden-onset severe chest or epigastric pain, often radiating to the back or shoulder, after repeated episodes of retching or vomiting in association with over-indulgence in food and alcohol.”
    Most presentations of Boerharve’s syndrome are atypical and the diagnosis often requires a high index of suspicion – usually an “oesophogram” of some sort is required.
    In about 1 in 4 cases there is no history of vomiting!

    Q4. What is the Mackler triad?

    The Mackler triad consists of:

    1. vomiting
    2. lower thoracic pain
    3. subcutaneous emphysema

    Although it supposedly defines the classic features of Boerhaarve’s syndrome it is probably not worth knowing because it is rarely found and is of negligible clinical utility in the real world.

    Q5. Outline the management of this condition.

    This a a highly lethal condition – it is essentially 100% fatal if left untreated. Overall mortality is about 30%.

    The cornerstones of management are:

    • aggressive resuscitation
    • early surgical intervention
    • broad-spectrum antibiotics

    Resuscitation should be followed by prompt surgical intervention (call the thoracic surgeons!). The time between onset of symptoms and surgery is the greatest predictor of patient survival.

    • best outcomes if surgery is performed <12 hours from onset.
    • mortality probably increases to ~50% at 24 hours, and to ~90% at 48 hours.

    Empirical antibiotics are indicated and should be broad spectrum to cover gram positives (including enterococcus), gram negatives and anaerobes. Some also advocate antifungal cover with fluconazole in initial empirical treatment as Candida is commonly grown from drain fluid in these patients (sometimes I give this and sometimes I don’t and I’m not sure whether doing this is a good idea or not).

    Conservative management (i.e. without surgery) may be appropriate in some situations:

    • presentation >48 hours
    • debilitated premorbid condition
    • a contained rupture, with minimal symptoms and negligible clinical evidence of sepsis.

    Although there is little consensus for the management of this rare condition, one suggested treatment algorithm is:

    boerhaarves mgt Pulmonary Puzzle #003

    Filed Under Chest X-Ray, Clinical Case, Gastroenterology, General Surgery, Intensive Care, Respiratory Tagged With boerhaave syndrome, cxr, ruptured oesophagus

    Letting Go

    November 25, 2009 By Chris Nickson 7 Comments

    A few experiences in the last week or two have reminded me of the importance of Peter Safar’s Laws for the Navigation of Life:

    Law 20. Death is not the enemy but occasionally needs help with timing.

    Sometimes some of us seem to forget that for all of us the time will come one day.

    Death is an inescapable fact of life. Really when it comes to death, our job as doctors is to help ensure that people die in the ‘right’ order – not too soon, not too late. Sometimes this means we shouldn’t intubate, we shouldn’t place central lines, we shouldn’t insert vascaths and start renal replacement therapy, we shouldn’t start myriad infusions of inotropes and vasopressors, and we shouldn’t take the patient to the operating theatre. Recognising that the time is right for a particular patient can save a lot of distress and suffering – for the patient, the patient’s family and friends, as well as the medical and nursing staff caring for the patient.

    When this goes wrong, sometimes the only antidote is black humo(u)r. Here are some of the worst antidotes I know:

    Q. What is the difference between a Rottweiler and an Oncologist?
    A. After you’re dead, the Rottweiler will let you go.

    Q. How can you recognise a Hematolgist?
    A. Look for the scorch marks on his hands from trying to hold back the coffin as it goes into the crematorium.

    The oncologist scratched his head. After 19 cycles of chemotherapy, his patient still wasn’t getting better. In fact he was worse.

    “Let’s try one more cycle of chemotherapy”, he said.

    After the 20th cycle the patient went to see the Oncologist again. The patient was so tired and listless he couldn’t speak. His skin and eyes were yellow, he was unable to eat or defecate, his face was puffy and he couldn’t pass urine.

    The Oncologist pondered his options. “I think we should try one more cycle of chemotherapy”, he said.

    The patient died. The Oncologist left the funeral perplexed. “Maybe we gave up too soon”, he muttered to himself. “Maybe one more cycle of chemotherapy will bring him back”.

    The Oncologist dug into the freshly turned soil with his shovel. Finally he reached the coffin. With sweat dripping from his brow he forced the coffin door open. Inside was empty. “What? Where is my patient?”, the Oncologist exclaimed. He frantically searched inside the coffin and finally found a note.

    The note said, “Gone for dialysis”.

    Hat tips to all those who have shared their morbid senses of humo(u)r with me over the years. And to all the oncologists, hematologists and nephrologists out there – no hard feelings – you’re still the among the smartest, most dedicated and caring docs out there.

    Filed Under Intensive Care Tagged With Death, Hematology, humour, Medical Humor, Nephrology, Oncology, peter safar, Renal
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