The unexpected killer - "Burkholderia Pseudomallei"

In this episode, lets discuss the unexpected killer - Melioidosis…

Check out the show notes as you listen to the podcast.

MELIOIDOSIS

The widow maker lesion

Wellens' Syndrome

Wellens’ syndrome was first described by Prof Hein J.J. Wellens in 1982. It can be best described as a warning for an impending heart attack. As emergency physicians it is crucial for us to be able to recognise this ECG pattern. Recognition of this ECG pattern can potentially prevent the myocardial infarction. 

It is important to understand that Wellens’ syndrome is not just an ECG sign alone but ECG signs in context with the clinical picture illustrated below.

Identification with examples

There are 2 types of Wellens’ waves:

• Wellens' with biphasic T waves and  - Figure 1
• Wellens' symmetrically inverted and deep T waves – Figure 2

Figure 1 (image courtesy - Lifeinthefastlane)

Figure 2 (image courtesy: Lifeinthefastlane)

 Diagnostic criteria for Wellens:

1.   Deeply inverted or biphasic T waves in V2-V3 sometimes extending from V1 to V6

2.   Isoelectric or slightly elevated ST segment (< 1mm)

3.   No pathological precordial Q waves

4.   Preserved precordial R wave progression

5.   Recent history of Angina

6.   ECG pattern in pain free state

7.   Normal or slightly elevated serum cardiac markers

Clinical Importance

• Signifies critical left anterior descending artery occlusion and high risk for extensive myocardial infarction
• About 75% of patient with this ECG finding have AW STEMI within < 2 weeks. 
• These patients may or may not have active chest pain at presentation and the cardiac enzymes may be normal or elevated
• These patients are not fit for stress tests as they are too high risk for a large myocardial infarct

                                           

What should you do when you encounter this finding?

Get cardiology involved and push for a timely angiography. Medical Management is usually ineffective for these lesions, these are best managed with PCI.

Key Points:

• Watch out for Wellen's waves routinely (esp biphasic T waves)
• This subset of patients may not have chest pain and normal cardiac biomarkers.
• Don't send them for a stress test. 
• Discuss with Cardiology for urgent/emergent PCI

References

1. de Zwaan C, Bar FW, Wellens HJ. Characterstic electrographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982 Apr; 103: 730-6

2.  Rhinehardt et al. Electrographic manifestations of     Wellens Syndrome. Am J of Emergency Medicine 2002 Nov; 20(7):638-43

3. Liu Mao et al. For Physicians: Never forget the specific ECG T- wave changes of Wellens syndrome. International Journal of Cardiology. 2013 July 15;167(1)

4. Tandy TK et al. Wellens’ Syndrome. Annals of Emergency Medicine. 1999 Mar; 33(3): 347-51

More Learning 

1.   lifeinthefastlane.com

2.   SSmith’s ECG Blog  

3.   Ecgweekly.com

                 

Author
Dr. Akshay Kumar MBBS, MRCP
Twitter: @akshay2111            
Senior Resident
Department of Emergency Medicine
All India Institue of Medical Sciences
New Delhi

Edited by: Lakshay Chanana

Subarachnoid Hemorrhage

A missed diagnosis could be the ‘worst headache’ of our lives!

Let’s do a quick review of one of the major neurological emergencies - the deadly subarachnoid hemorrhage.  Although traumatic SAH is the most common type presenting to the ED, in this review we will be dealing with only SAH of non-traumatic etiology as diagnosis and management. This in the ED is of paramount importance and any delay is associated with significant morbidity and mortality.

What and where?

Leakage of blood/bleeding into the subarachnoid space (between arachnoid mater and pia mater). The picture below should make things easier to understand.

Etiology:

• Rupture of ‘Berry’ aneurysms in the circle of Willis (commonest cause ~ 85%)
• Arteriovenous malformation
• Rupture of the mycotic aneurysms
• Tumors
• Connective tissue disorders
• Idiopathic ( also translated as ‘’WE STILL HAVE NO CLUE’’) ~20%
• Drugs

Risk factors for SAH:

• Past H/O SAH
• Hypertension
• Smoking
• Excessive alcohol consumption
• Polycystic Kidney disease
• Family history of SAH*
• Marfan’s syndrome, Ehler-Danlos syndrome type 4
• Coarctation of aorta

*2% of the family members of patients will develop SAH. Risk increases with increasing number of family members having SAH.

History and Clinical Features:

Headache is the most common presenting complaint. The classic descriptions include,

·      “The worst headache of my life”, “my head is exploding”.

·      ‘Thunderclap headache’ – Like a blow to the back of head.

      Severe headache of sudden onset that reaches maximal intensity within minutes.

      Severe headache with change in the character/difference in intensity or of unique quality when compared to past headaches. This is particularly important in patients who are having chronic headache (ex: Migraine). Never ignore a headache that’s ‘different’, ‘never felt before’, ‘worst’ or not subsiding with ‘usual’ medicines, with associated symptoms (especially in a patient with chronic headache syndrome where the chances of missing a diagnosis is more) à need further investigation.

·    ‘Warning headaches’ may precede the onset of SAH.

·    In ~25% patients, exertional activities may precede the event. May also be preceded by sexual intercourse, exercise, defecation (all activities which increase BP)

     Other associated features may include,

•       Neck pain/stiffness
•       Vomiting/Nausea (must increase your suspicion)
•       Syncope (Yes, SAH too can present with syncopy!)
•       Altered mental status
•       Seizures, posturing
•       Focal neurological deficits
•       Dilated unequal pupils, Unilateral eye pain, papilledema.
•       Fundoscopy may reveal subhyaloid hemorrhages*

*Pathognomonic of SAH in the absence of blunt trauma; but present only in about 11%-33% patients

Differential diagnosis:

• Intracerebral hemorrhage
• Cerebral venous thrombosis
• Ischemic stroke
• Meningitis/Encephalitis
• Coital cephalgia
• Metabolic abnormalities
• Intracranial tumor
• Primary headache syndrome (ex: Cluster headache, migraine, etc.)

Always have a high degree of suspicion when patients who are known to have primary headache syndromes present to the emergency department with headache that’s ‘different’ from the previous episodes or the headache that’s not responding to their usual medications.

Investigations and diagnosis:

Initial diagnostic modality of choice in a patient with suspicion of SAH is non-contrast CT pf the head. Sensitivity of CT is highest shortly after the onset of symptoms and ~98% when performed within 12 hours of onset. Sensitivity of CT reduces over time. In addition, anemic patients are more likely to have false negative CTs.

According to the guidelines, when SAH is suspected and if the CT is normal, a CSF analysis has to be done to look for Xanthochromia (Yellow appearance of CSF due to breakdown of hemoglobin into bilirubin – after 12 hours of onset of symptoms) and RBC count. (Measuring RBC count is not followed strictly in all centers as many studies have shown that these are not very reliable indicators of SAH and is time dependent. Local/departmental protocols can be followed in this regard.)

SAH suspected + Positive CT = SAH

SAH suspected + Negative CT + Positive CSF findings = SAH most likely

SAH suspected + Normal head CT + absent xanthochromia and zero or few RBCs in CSF = SAH almost ruled out.

Gold Standard for diagnosis is Cerebral Angiography

Labs: The SAH checklist for the first hour of presentation includes:

1. Brain imaging
2. Labs: CBC, PT, APTT, Electrolytes, Creatinine, Troponin, Toxicology screen
3. 12-Lead ECG 

Blood glucose level has to be checked to rule out the potentially reversible cause of symptoms.

ECG may show Tall T waves, ST depression, Giant T wave inversions secondary to raised ICP, QT prolongation and arrhythmias.

ECHO may show ‘neurogenic cardiomyopathy’: “Approximately 20% to 30% of patients with SAH manifest a secondary cardiomyopathy and/or regional wall motion abnormality, which is usually reversible in the absence of underlying obstructive CAD. This entity has been referred to as neuro-cardiogenic stunning and neurogenic stress cardiomyopathy”

(Read more about stress cardiomyopathy from the original article here à http://circ.ahajournals.org/content/118/4/397.full )

Troponins may be raised.

Patients may exhibit hyponatremia due to SIADH or cerebral salt wasting.

CXR may show neurogenic pulmonary edema.

Coagulation profile may be deranged if the patient is anticoagulated.

MRI, CTA are not routinely done. May be helpful in special circumstances and this has to be discussed with the neurology/neurosurgery teams for a consensus. CTA may be helpful for diagnosis of aneurysms.

Grading of SAH: There are different systems of grading based on clinical features, GCS and CT findings. These grades are used as predictors of prognosis. The most commonly used grading systems are

Hess and Hunt grading system

WFNS scale:

WFNS (World Federation of Neurosurgical Society) scale

Grade 1 – 70% survival rate                                 Grade 2 – 60% survival rate

Grade 3 – 50% survival rate                                 Grade 4 – 40% survival rate

Grade 5 – 10% survival rate    

        

Click on this link for more on other grading systems in SAH: http://lifeinthefastlane.com/ccc/subarachnoid-haemorrhage-grading-systems/

Complications of SAH

• Re-bleeding: Risk is highest in the first 24 hours.
• Hydrocephalus: About 30% develop in the first 3 days.
• Neurogenic pulmonary edema
• Aspiration pneumonia – Sepsis.
• Myocardial infarction, arrhythmias, LV dysfunction and neurogenic cardiomyopathy.
• SIADH à Hyponatremia: Most common 3days – 14days.
• Vasospasm: Most common 2days – 3 weeks following SAH.

ED Management of SAH and complications:

Definitive therapy is the obliteration of the aneurysm by clipping or endovascular coiling as soon as possible.

Airway and breathing:

Adequate oxygenation is very important. Aim for SpO2 > 94%. Aim for PaCO2 within the normal range.

Consider intubation and mechanical ventilation if:

•       Airway not patent.
•       Hyperventilation or hypoxia not responding to supplemental oxygen.
•       Anticipated deterioration or transfer to another center.

Tape the endotracheal tube in place rather than tie it to avoid increases in ICP

Consider RSI with drugs, which do not cause hypotension (Ketamine, Etomidate). Also try and do a quick neurological examination prior to RSI.

Other simple measures to reduce ICP:

Head end elevation

No IJ lines

Circulation:

Avoid hypotension. But also make sure that BP is not ‘very high’. There’s lack of adequate data regarding BP control in SAH patients. There is some data that suggests a higher rate of re-bleeding with SBP > 160mmHg.  So try to maintain the MAP between 90-110mmHg (Coming down up to 160/90 appears pretty safe).  IV Labetalol can be used as infusion or can be given intermittent doses.

The idea is to strike a balance between risks of stroke – HTN associated rebleeding – maintenance of cerebral perfusion pressure.

Blood sugars: Maintain normoglycemia.

Seizures: Possibly seen due aneurysm rupture and increased ICP. Use anticonvulsants for treating actual seizures. Use of prophylactic anticonvulsants is controversial; but AHA and NCS (Neurocritical care Society) suggest consideration of anti-convulsants in the immediate post hemorrhage period. Use of Levetiracetam may be considered as use of phenytoin is associated with worse long term outcomes.

Coagulopathy: Mainly seen in patients on Warfarin therapy. Patients with INR > 1.4 should be treated with combination of FFPs, Vitamin K and PCC. Low platelet count below 50,000 is treated with platelet transfusions. If they are on antiplatelets, reverse them with platelet transfusions in consultation with hematology.  

Pain: Short acting IV analgesics like Fentanyl can be used. Help the patient avoid straining, Valsalva and coughing.  Fentanyl is probably a better choice here as compared to Morphine, as the latter cause histamine release, that can lead to vasodilatation and a bump in ICP. Small doses of Lorazepam might help to relieve anxiety if any. But be cautious that overdose of medications does not mask change in mental status.

Vasospasm: Can be treated with Nimodipine 60mg, PO/NGT every 4^th hourly. The use of nimodipine is associated with improved overall outcomes. This should be initiated within 96 hours of symptom onset unless contraindicated.

Avoid hypothermia and hyperthermia. Aim for normothermia. This can be achieved by appropriate usage of warming/cooling blankets, mechanical warmers, antipyretics.

Aspiration and sepsis: Early antibiotics and fluid management if suspected. Follow sepsis guidelines.

Hydrocephalus: May require EVD insertion. Consult Neurosurgery team early.

Communication and referrals:

• Always involve neurology and neurosurgery team early.
• Convey the present condition of the patient, CT finding, absence/presence of hydrocephalus, grading, present management, expected course of events and further investigations like CT angiography that might be required when talking to the specialist.
• Transfer to the appropriate center if your center doesn’t have neurosurgical facilities.

Take home points:

•       Ask them "Is it different from their previous headaches".
• Ask for any headache preceding syncope!
• Non contrast CT is highly sensitive if done within early hours of onset of symptoms and a CSF analysis confirms the diagnosis if CT is negative.
• Reverse anticoagulants when INR > 1.4 and Antiplatelets when counts < 50,000.

                 Author

                 Dr. Apoorva Chandra

                 Twitter: @apoorvamagic  
                 Resident, Emergency medicine         

                 Apollo Health City, Hyderabad                                                         

                 apoorvamagic@gmail.com

Further reading and references:

1. Emergency Neurological Life Support (ENLS) guidelines for SAH: http://enlsprotocols.org/files/SAH.pdf

2.  A Guideline for Healthcare Professionals From the AHA/American Stroke Association: http://stroke.ahajournals.org/content/early/2012/05/03/STR.0b013e3182587839.full.pdf

3.    Neurogenic Cardiomyopathy:
-       http://circ.ahajournals.org/content/118/4/397.full
-       http://www.ncbi.nlm.nih.gov/pubmed/17290097

4.    Neurogenic pulmonary edema:
-       http://lifeinthefastlane.com/ccc/neurogenic-pulmonary-oedema/
-       http://www.ccforum.com/content/16/2/212
-       http://www.ncbi.nlm.nih.gov/pubmed/21775947

5.    Blood pressure control for acute ischemic and hemorrhagic stroke.
http://www.ncbi.nlm.nih.gov/pubmed/22322257

6. HOW TO BE A CLINICAL ROCK STAR MANAGING SUBARACHNOID HEMORRHAGES
http://www.emdocs.net/clinical-rock-star-managing-subarachnoid-hemorrhages/

7.  For more radiology on SAH: http://radiopaedia.org/articles/subarachnoid-haemorrhage