concave considerations…

the case.

37 year old female presents to your Emergency Department complaining of shortness of breath and bilateral thigh pain after vomiting for one week.

It’s a busy day in the department, so whilst a bed is being organised the nursing staff have obtained IV access and taken the following venous blood gas…

  1. Moderate metabolic acidosis:
    • HCO3 16, BE -10.
    • Partially compensated with a pH 7.24
    • Exp pCO2 = (1.5x 16) + 8 = 24 + 8 = 32.
    • Actual = 39 (Likely due to VQ mismatch).
  2. High anion gap (Cl = 91)
    • 135 – (91+16) = 28
    • Delta ratio
      • = (28-12)/(24-16)
      • = 16/8
      • = 2 ∴pure HAGMA
  3. Severely elevated lactate: 9.8 mmol/L !!
    • DDx: sepsis, tissue ischaemia, medications…
  4. Moderately elevated serum creatinine
  5. Mild anaemia
  6. Mild hyperglycaemia
  7. Mildly low ionised calcium

The gas shows a high anion gap metabolic acidosis, specifically a lactic acidosis. This is likely driven by a Type 1 lactic acidosis due to tissue hypoxia and anaemia. Persistent vomiting is more likely to produce a metabolic alkalosis so this is not the driving force of this blood gas.

She is hypotensive at 90/60 mmHg and she is taken to the resuscitation bay where you meet her.

She rapidly states that she has heterozygous sickle cell disease.

Are all heterozygous patterns less severe?

This lady was HbS/β0 thalassaemia compound heterozygous and of similar clinical severity to HbSS disease (see the table below for more detail).

Sickle cell disease genotypes. (Source: Wasil, 2011 – Ref#1)

She has had non-bilious vomiting for the past 5 days which she puts down to a viral gastroenteritis that she caught from her daughter. During this time she has likely fallen behind in hydration as she didn’t seek help until she “couldn’t bear the pain.” Today, she started to have breathing difficulties.

She describes a mild headache plus bilateral deep burning pain in her thighs. She is on hydroxyurea, denies pregnancy and states she has had all her vaccinations.

On examination:

  • A. Patent & protected.
  • B. Tachypnoeic to 32 breaths per minute. SpO2 93% on 15L via non-rebreather mask.
  • C. Tachycardic  (HR 121/min, sinus), Blood pressure 102/82 after an initial fluid bolus. Peripherally shut down and cool to touch. Dry mucosa.
  • D. GCS15, PEARL, no focal neurology.
  • E. Temperature 35.3*C. Appears lethargic++.
  • Other:
    • Abdomen soft with a mildly enlarged liver
    • No splenomegaly to suggest aplastic crisis.
    • No warmth in the leg joints to suggest sceptic joint or soft-tissue infection.

What conditions specific to sickle disease would account for her symptoms?


Acute chest syndrome.

The exact pathogenesis of acute chest syndrome (ACS) is unclear and is probably multifactorial. It is essentially an ARDS-subtype and clinically diagnosed with pulmonary alveolar consolidation.

Proposed mechanism for acute chest syndrome & vasoocclusive crisis in Sickle Cell Disease. (Source: Novelli, 2016 Ref#2)

  • Pulmonary infection:
    54% of patients admitted for ACS will have an infectious agent identified. Community acquired pathogens are most common. Despite increased risk of encapsulated bacteria due to functional hyposplenism these are isolated in only 10% of patients.
  • Fat emboli:
    80% are involved with vasoocclusive (VO) crisis and this lends itself to the theory that fat emboli with secondary ARDs may be the underlying pathology. Studies show 44% of patients that underwent a bronchoscopy during an ACS crisis had lipid-laden alveolar macrophages.
  • Haemolysis:
    Acute haemolysis coexists with a rise in LDH and dropping Hb. Mice models have shown that heme is necessary and sufficient to induce ACS.
  • Pulmonary infarction/PE:
    Given the prothrombotic state that sickle-cell patients are in during an acute crisis, they are susceptible to PE and lung parenchymal infarction. Literature suggests that PE is under diagnosed in this population despite the incidence actually being higher.

Vasoocclusive crisis (bony crisis).

“Sickling” causes microvascular entrapment of erythrocytes and leukocytes which lead to ischaemia. This leads to a subsequent inflammatory reaction that worsens the environment and encourages further sickling. The end product is necrosis that is felt as pain.

Mechanisms of vasoocclusion in Sickle Cell Disease
(Source: Montalembert, 2008 – Ref#3)

In this specific patient:

  • Sepsis:
    These patients are at risk of overwhelming sepsis. They have hypo/asplenism; so are vulnerable to encapsulated bacteria. She presented hypotensive & has an elevated lactate and should therefore receive empiric broad-spectrum antibiotics.
  • Cerebrovascular events:
    She had a mild headache but no focal neurological deficit. Ischaemic stroke was considered but the headache was thought to be due to skull bone vasoocclusive symptoms.
  • Multi organ failure:
    She had already developed an acute kidney injury and ARDS. During her admission she had deranged LFTs that normalised during her stay.
  • Septic arthritis:
    On inspection the legs were bone pain. Sickle cell patients (more common in paediatric patients) are at higher risk of sceptic arthritis.

  1. Oxygen:
    • Aim to maintain saturations >97%.
    • The peripheral pulse oximetry probe is unreliable and an ABG on room air should guide treatment (this also helps prognosticate for ACS/ARDS).
  2. Intravenous fluid:
    • Traditionally 1.5x maintenance fluid is required.
  3. Analgesia:
    • Pain crises are very painful and usually patients have tried opioids and escalating pain management regimens prior to attending hospital.
    • Morphine PCA (or equivalent) is usually required.
  4. Antibiotics:
    • Infection is a leading cause of ACS.
    • In this case we gave intravenous ceftriaxone.
  5. Investigations:
    • Biochemistry (Electrolytes, LFTs, CMP, βHCG)
    • Group & hold
    • Haemolytic screen, HbF
    • Infectious screen including Parvovirus B12, EBV/CMV & blood cultures
    • CXR
    • Arterial blood gas (preferably on room air)

Arterial blood gas (FiO2 0.60). A-a Gradient >170, metabolic acidosis, elevated lactate.

Anaemia with elevated Bilirubin & LDH consistent with haemolysis. Elevated WCC with neutropenia (?sepsis). Elevated creatinine (moderate AKI, ?pre-renal).


There is usually a 24 to 72 hour delay in chest findings in a crisis. So a patient can have acute chest syndrome with a lag in radiological findings. It is a clinical diagnosis requiring the presence of hypoxia and dyspnoea to herald ACS.

In severe ACS/VO occlusive crisis after initial ED stabilisation the definitive treatments is plasma exchange. Essentially it aims to minimise the HbS load to <30% ( this number is institution dependent and some say <20%).

…..this patient had 8 units of PRBC and responded really well both clinically and biochemically. Her HbS went from 47% to 20%

This lady was Caucasian and presented with a sickle crisis most likely from dehydration secondary to her week of vomiting. She had a heterozygous phenotype that may have given some people false reassurance of her severity subtype. She got exchanged 8 units within 3 hours of presentation due to early involvement of Haematology and Intensive Care. This lady needed significant amounts of analgesia (at home prior to her presentation and in the Emergency Department). From a practical standpoint she had multiple antibodies in her blood and this made accessing suitable blood one of her rate limiting factors.

ACS carries a high risk of respiratory failure with 13% of patients requiring mechanical ventilation and a mortality rate of 9%. It is associated with prolonged hospitalisation and decreased overall prognosis. It remains the most common cause of death for this patient population. Ultimately, sickle cell disease is a terminal illness and these patients can get unwell quickly.

Fortunately this lady spent 48 hours in the ICU needing only the initial plasma exchange. She spent further time on the general ward in hospital and had a CTPA that showed a sub-segmental PE and was discharged with ongoing outpatient Haematology followup.

  1. Wasil, J (2011) Epidemiology of sickle cell disease in Saudi Arabia. Annals of Saudi Medicine 33(3):289-293.
  2. Novelli, E., Huynh, C., Gladwin, M.,Moore, C., Rangi, M(2012). Pulmonary Embolisation in Sickle Cell Disease: A case-control Study. Journal of Thrombosis Haemostasis. May 10(5):760-7663.
  3. Gladwin, M., Vinchinsky, E (2008) Pulmonary complications of Sickle Cell Disease. NEJM 2008: 359:2254-2265.
  4. EM: RAP: July 2017- Jonathan’s story. Dr Jessica Mason
  5. Gladwin, M., Vichinsky, E (2008) Pulmonary complications of Sickle cell Disease. NJEM 359:2254-65
  6. Golman & Schafter. Goldman’s Cecil Medicine 24th edition. Ch166 Sickle cell disease and other haemoglobinopathies.
  7. Montalembert (2008) Management of sickle cell disease. BMJ v327
  8. Novelli, E., Gladwin, M (2016) Crises in sickle cell disease. Chest 149(4):1082-1093
  9. Yawn, B., Buchanan, G., Afenyi-Annan, A (2014). Management of Sickle Disease. Summary of the 2014 Evidence-Based Report by Expert Panel Members JAMA 2014; 312(10):1033-1048


Author: Courtney Peros
Web editing: Chris Partyka

canary in the mine…

the case.

16 year old female presents to your Emergency Department after falling from her mountain bike on a nearby track. As she fell to the ground, she reports landing on the handlebars which struck her upper abdomen.

She describes navigating a difficult section of a familiar track when her front wheel impacted a large tree root causing a loss of balance and the subsequent accident. A handlebar from her bike impacted her upper abdomen causing immediate pain and a moderate sized contusion. She has vomited once since the injury.

She otherwise appears to be ok.
– Was wearing a helmet at the time, did not lose consciousness and recalls all events.
– Has no dyspnoea, painful breathing or chest pain.
– Has no extremity pain, swelling or deformity.

She has no significant past medical history, takes no regular medications and has no known allergies.

On examination, she looks well but is in moderate pain.

  • A. patent & protected.
  • B. No chest wall crepitus, tenderness or emphysema. Respiratory rate 18/min. SaO2 98% (room air) Clear lung fields.
  • C. Warm and well perfused. Pulse rate 92 per minute. Blood pressure 110/68. No active external haemorrhage or long bone fractures.
  • D. GCS 15. Moving all 4 limbs. Pupils 5mm and reactive to light.
  • E. Well circumscribed abdominal wall contusion (~3 cm diameter) in the epigastrium, just left of the midline. She has moderate tenderness on deep palpation with voluntary guarding, but no rebound or percussion tenderness.

Your colleagues place a cannula and administer some analgesia.
During that time you grab your ultrasound …

The remainder of her images are normal.

Free fluid at the caudal liver edge & the splenorenal interface.

In the unstable patient with blunt abdominal trauma, the test characteristics of the FAST scan are impressive (Sn 73-88%, Sp 98-100%). However, in patients with penetrating trauma & in those with stable haemodynamics, this sensitivity falls away to 50% or less. This brings into question whether or not the FAST scan still has a role in the bedside assessment of these patients, where advanced imaging with contrast CT provides a greater level of diagnostic accuracy.

Here is a talk that I gave at the 2017 SWAN Trauma Conference on the role of the FAST scan in stable blunt trauma patients…

& here are the accompanying slides…

Despite her normal haemodynamics, this positive FAST scan signifies that she is carrying a significant intraabdominal injury & a high likelihood of clinical deterioration.

You notify your surgical colleagues & arrange an urgent abdominal CT…

  • Grade III splenic laceration (predominant grade II anterior laceration with other small subcapsular lacerations).
  • Intra parenchymal vascular injury is noted.
  • Small volume of free fluid.

Whilst your patient remains stable, with normal vital signs, the decision is made to proceed to interventional radiology. Here she undergoes selective angio-embolisation of a branch of the splenic artery.

She is admitted to the High Dependency Unit for overnight observation, where her haemodynamics and haemoglobin remain stable. Her recovery is uneventful and is discharged well 5 days later.

  1. Natarajan B, Gupta PK, Cemaj S, Sorensen M, Hatzoudis GI, Forse RA. FAST scan: is it worth doing in hemodynamically stable blunt trauma patients? Surgery. 2010; 148(4):695-700; discussion 700-1. [pubmed]
  2. Dammers D, El Moumni M, Hoogland I, Veeger N, ter Avest E. Should we perform a FAST exam in haemodynamically stable patients presenting after blunt abdominal injury: a retrospective cohort study Scand J Trauma Resusc Emerg Med. 2017; 25(1). [pubmed]
  3. Lee BC, Ormsby EL, McGahan JP, Melendres GM, Richards JR. The utility of sonography for the triage of blunt abdominal trauma patients to exploratory laparotomy. AJR. American journal of roentgenology. 2007; 188(2):415-21. [pubmed]
  4. Liu K. FAST Scan: Is it Worth Doing in Hemodynamically Stable Blunt Trauma Patients? The Journal of Emergency Medicine. 2011; 40(5):607-608. [link]
  5. Cho Y, Judson R, Gumm K, Cho Y, Santos R, Walsh M, et al. Blunt Abdominal Trauma. Trauma Service Guidelines: The Royal Melbourne Hospital; 2012. [link]
  6. Fleming S, Bird R, Ratnasingham K, Sarker S, Walsh M, Patel B. Accuracy of FAST scan in blunt abdominal trauma in a major London trauma centre International Journal of Surgery. 2012; 10(9):470-474. [link]
  7. Hsu JM, Joseph AP, Tarlinton LJ, Macken L, Blome S. The accuracy of focused assessment with sonography in trauma (FAST) in blunt trauma patients: Experience of an Australian major trauma service Injury. 2007; 38(1):71-75. [link]
  8. Bowra J, Forrest-Horder S, Caldwell E, Cox M, D’Amours SK. Validation of nurse-performed FAST ultrasound. Injury. 2010; 41(5):484-7. [pubmed]
  9. Behboodi F, Mohtasham-Amiri Z, Masjedi N, Shojaie R, Sadri P. Outcome of Blunt Abdominal Traumas with Stable Hemodynamic and Positive FAST Findings. Emergency (Tehran, Iran). 2016; 4(3):136-9. [pubmed]
  10. Matsushima K, Frankel HL. Beyond focused assessment with sonography for trauma: ultrasound creep in the trauma resuscitation area and beyond. Current opinion in critical care. 2011; 17(6):606-12. [pubmed]
  11. Richards JR, McGahan JP. Focused Assessment with Sonography in Trauma (FAST) in 2017: What Radiologists Can Learn Radiology. 2017; 283(1):30-48. [link]
  12. The Use of FAST Scan by Paramedics in Mass-casualty Incidents: A Simulation Study Prehosp. Disaster med.. 2014; 29(06):576-579. [link]

cracking under pressure…

the case.

a 44 year old male presents to your Emergency Department with severe, crushing retrosternal chest pain. He reports that the pain started suddenly approximately one hour ago whilst at rest.

It is described as a retrosternal pressure or tightness which radiates up to his neck, through to the back & down towards his umbilicus.

The pain is associated with severe palpitations. There is no associated dyspnoea, cough or haemoptysis. There have been no syncopal or near-syncopal episodes and he has no neurological symptoms. He has never had pain like this before.

Past Medical History:

  • Hypertension
  • Hypercholesterolaemia


  • Simvastatin
  • Ezetimibe

No significant social history.

On examination. 
He looks unwell. He is profoundly clammy and diaphoretic.

  • A: Patent & protected.
  • B: Tachypnoeic (28 breaths per minute), minimal work of breathing. SaO2 95% (RA). Chest clear to auscultation.
  • C: Pulse rate 135 per minute, Blood pressure 190/110 (no differential between left & right arms). Good peripheral pulses without pulse deficit. Heart sounds dual without murmurs or rub.
  • D: GCS 15. Equal and reactive pupils (4mm). Moving all 4 limbs. No focal motor or sensory changes.
  • E: Temperature 37.7*C. Blood glucose 8.2 mmol/L.

You can’t help but notice that he has a new dressing over his left deltoid. When you enquire about this, he tells you that earlier that day he underwent an elective resection of a skin lesion under general anaesthetic at a nearby hospital. This was apparently an uneventful procedure & recovery and he was discharged home only a few hours ago.

  • Narrow complex (sinus) tachycardia at a rate of ~140 beats per minute.
  • Normal axis.
  • ~1mm of ST segment elevation in aVR with diffuse, widespread ST segment depression (V3-6, I & aVL)
  • PR & QRS intervals normal.
  • Prolonged QT interval.

Differential diagnoses include;
(1) left main coronary artery occlusion
(2) proximal LAD occlusion
(3) severe triple vessel disease
(4) diffuse sub-endocardial ischaemia (myocardial O2 supply/demand mismatch)

  1. Severe metabolic acidosis:
    • HCO3 13, BE -15.
    • Uncompensated with a pH 7.17
    • Exp pCO2 = (1.5×13) + 8 = 20 + 8 = 28.
    • Actual = 37, therefore a contributing relative respiratory acidosis.
  2. High anion gap (Cl = 102)
    • 141 – (102+13) = 26
  3. Severely elevated lactate: 15mmol/L !!
    • DDx: sepsis, hyperadrenergic state, ingestion, malperfusion/ischaemia, MH
  4. Severe hyperglycaemia: 28 mmol/L
    • ?new onset diabetes ?stress response
    • Are there ketones contributing to the acidosis?? In this case, they were normal.
  5. Mild hypokalaemia:
    • K 3.8mmol/L, however when corrected for acidosis is more likely <3!
  6. Mildly elevated serum creatinine.
    • ?acute vs chronic
    • ?contributory vs incidental finding
  7. Hb 170
    • ?haemoconcentration 

  • Normal cardiomediastinal contour.
  • Clear lung fields without collapse or consolidation.
  • No pleural effusions.

  • Acute coronary syndrome
  • Aortic dissection
  • Hypertensive crisis – but why?
    • Cardiovascular
    • Renal
    • Endocrine
    • Haematologic
    • Intoxication/ingestion
  • Malignant hyperthermia (cases of delayed onset MH have been reported)
  • Sepsis
  • Thyroid storm
  • Intoxication/ingestion
    • Sympathomimetic toxidrome
    • Anticholinergic toxidrome
    • Serotonin syndrome
    • Neuroleptic malignant syndrome
    • Salicylate toxicity
    • Methylxanthine toxicity

  • IV access
  • Analgesia
    • Titrated intravenous opiates is suitable (eg. Fentanyl 50mcg IV q5-10mins)
  • Nitrates:
    • Easier (& quicker) to start with a sublingual tablet followed by infusion for blood pressure control & reduction of ongoing ischaemic chest pain
  • Detect and correct electrolyte derangement especially potassium

With a strong clinical suspicion for aortic dissection, antiplatelet therapy & anticoagulation are withheld and a CT Aortogram is arranged urgently…

Did you see it? Did you see it?

Upon return from radiology, he continues to complain of severe retrosternal pain…

His pulse remains 136 per minute with a blood pressure of 196/118 mmHg despite your GTN infusion now running at 250 micrograms per minute.

The nurse looks at you and asks, “What are we going to do now??


Phaeochromocytoma is a catecholamine-secreting neuroendocrine tumour (a paraganglioma), most frequently arise from the chromaffin cells of the adrenal medulla.


  • Incidence is very low ~2 people/million/year.
  • Most common between ages of 20 and 50 years.
    • 50% of cases are diagnosed only at post-mortem examination.
  • “10% rule”
    • Bilateral in 10% of cases
    • 10% are extra-adrenal
    • 10% are malignant
    • ~10% are found in children
    • ~10% are familial
  • Phaeochromocytomas are the secondary cause of hypertension in 0.1% of hypertensive patients.
  • A proportion of patients are diagnosed at the time of incidental surgery when induction of anaesthesia may precipitate a hypertensive crisis.
    • Mortality in this instance is close to 80%.

Clinical presentation.

Classically, phaeochromocytoma manifests as spells with the following 3 characteristics…

These spells may or may not be associated with severe hypertension.

Typical patterns of the spells are as follows:

  • Frequency may vary from monthly to several times per day
  • Duration may vary from seconds to hours
  • Over time, spells tend to occur more frequently and become more severe as the tumour grows.

The typical features of phaeochromocytoma are predominantly cardiovascular:

    • Paroxysmal (~45%)
    • Sustained (50%)
    • NB. ~5% are normotensive
  • Palpitations and tachycardia
  • Headaches
  • Tremor
  • Sweating
  • Anxiety
  • Chest pain (± myocardial infarction)
  • Cardiac failure (± acute pulmonary oedema)

Other symptoms include;

  • Nausea
  • Weakness
  • Anxiety or a sense of doom
  • Epigastric pain
  • Flank pain
  • Constipation


Clinical suspicion remains the single most important factor in
the identification of phaeochromocytoma.

Phaeochromocytomas can present as a component of familial syndromes (esp. thyroid cancers). It is important to be aware of this association.

Image courtesy of Alderazi et al.

Measurements of urinary catecholamines and their metabolites, metanephrines, over 24 hours have been the mainstay of biochemical diagnosis of phaeochromocytoma for many years (Sn 88%, Sp 99%).

Tests for catecholamines and their metabolites

  • Urinary catecholamines
  • Plasma catecholamines
  • Urinary fractionated metanephrines
  • Plasma free metanephrines (these appear to be the best single investigation)
  • Urinary vanillylmandelic acid

Clonidine suppression test
In patients with phaeochromocytoma, serum catecholamine levels will not decrease in response to clonidine (they are independent of neurogenic control).


  • CT scan (including dedicated adrenal study with washout)
  • MRI
  • Nuclear medicine (esp.I-123 MIBG)
  • PET scan

Check for alternate diagnoses:

  • Thyroid function (TSH, T4)
  • Plasma renin activity
  • Cortisol levels (plasma & urine)


Phaeochromocytoma is known for life-threatening acute hypertensive emergencies, as well as clinical consequences of long-lasting hypertension.

Spells or crises can result from a variety of precipitants including;

  • Postural changes, physical exertion, emotion
  • Certain foods or beverages (especially those with tyramine eg. cheese, beer, wine)
  • Direct tumour stimulation (abdominal pressure or injury)
  • Drugs/medication:
    • histamine, ACTH, metoclopramide, phenothiazine, TCAs or anaesthetic agents.

Organ-Specific Hypertensive Complications

  • Cardiac
    • Acute coronary syndromes (including myocardial infarction)
    • Cardiomyopathies (incl. Takotsubo)
    • Myocarditis
    • Heart failure including pulmonary oedema and cardiogenic shock
    • Dysrhythmias
  • Cerebrovascular
    • Stroke
    • Hypertensive encephalopathy
  • Vascular
    • Shock
    • Postural hypotension
    • Aortic dissection
    • Organ ischaemia
    • Limb ischaemia
  • Renal
    • Acute renal failure
    • Haematuria
  • Gastrointestinal
    • Intestinal ischaemia (necrosis or peritonitis)
  • Ocular
    • Acute blindness
    • Retinopathy
  • Multisystem failure
    This complication consists of multiple organ system failure

    • Fever over 40°C
    • Encephalopathy
    • Severe hypertension and/or hypotension
    • Pulmonary oedema
    • Anuric acute renal failure
    • DIC


Management of phaeochromocytoma-related emergencies depends on the symptoms; however, it should always include pharmacologic treatment to block the effects of high levels of circulating catecholamines and prevent life-threatening catecholamine-induced complications.

This review will not cover the pre-operative management of these patients.

  • Control of hypertension.
    • Rapidly acting α-1 antagonist:
      • Phentolamine: 0.5-1mg per minute in aliquots or via infusion.
    • Slowly acting non-competitive α-1 antagonist:
      • Phenoxybenzamine reserved for post-crisis care & pre-op optimisation
      • Prazosin 
    • Others:
      • GTN
      • Sodium nitroprusside
      • β-blockers (only after adequate α-blockade) – eg. atenolol or propranolol
      • Calcium channel blockers
  • Maintenance of circulating volume in the face of vasodilation.
    • IV fluid replacement
  • Control of atrial fibrillation.
    • Verapamil, diltiazem or amiodarone
  • Assessment of myocardial damage.
    • ECG
    • Echocardiography
    • Troponins
  • Seek and treat precipitating cause
  • Admit for further workup & operative planning

Definitive treatment is surgical removal and if complete resection is achieved, without metastases, then surgery is curative  in >90% of cases. Following this, hypertension usually resolves.

Following confirmation of the adrenal lesion, the patients blood pressure is managed acutely with a high-dose GTN infusion and aliquots of phentolamine. He is subsequently admitted to the Intensive Care Unit for ongoing short-term care.

Over the following 48 hours he is transitioned onto oral antihypertensives, in this case, prazosin.

His 24-hour urinary collection demonstrated;

Normal metanephrine < 0.40, Normal normetanephrine < 0.90.

A subsequent dedicated adrenal CT demonstrated an absolute washout of 79%.

Here is his I-123 MIBG scan…

The scan appearances in the right adrenal gland are most in keeping with a MIBG avid pheochromocytoma. There is no scan evidence of MIBG avid disease elsewhere in this study.

After 5 days in hospital, he was discharged home with ongoing specialist input. He later underwent a successful, elective surgical resection of his phaeochromocytoma & is doing well…

  1. Alderazi Y, Yeh MW, Robinson BG. Phaeochromocytoma: current concepts. The Medical journal of Australia. 2005; 183(4):201-4. [pubmed]
  2. Zuber SM, Kantorovich V, Pacak K. Hypertension in pheochromocytoma: characteristics and treatment. Endocrinology and metabolism clinics of North America. 2011; 40(2):295-311, vii. [pubmed]
  3. Myklejord DJ. Undiagnosed Pheochromocytoma: The Anesthesiologist Nightmare Clinical Medicine & Research. 2004; 2(1):59-62. [pubmed]
  4. Pacak K, Eisenhofer G, Ahlman H. Pheochromocytoma: recommendations for clinical practice from the First International Symposium. October 2005. Nature clinical practice. Endocrinology & metabolism. 2007; 3(2):92-102. [pubmed]
  5. Frederick MJ, Colwell AS. Acute hypertensive crisis secondary to pheochromocytoma during elective cosmetic surgery. Plastic and reconstructive surgery. 2015; 135(1):238e-9e. [pubmed]
  6. Bensghir M, Elwali A, Lalaoui S et al. Management of undiagnosed pheochromocytoma with acute appendicitis World J Emerg Surg. 2009; 4(1):35. [pubmed]
  7. Raut M, Kar S, Maheshwari A et al. Rare postoperative delayed malignant hyperthermia after off-pump coronary bypass surgery and brief review of literature Ann Card Anaesth. 2016; 19(2):357-362. [pubmed]