March 15, 2010

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Cardiovascular Curveball #006

March 15, 2010 By Paul Young 2 Comments

Consider a 49 year- old female with a history of smoking and two weeks of increasing shortness of breath. She is being treated for pneumonia on the ward for three days but getting worse. An ICU review is performed on the ward and the following ECG is obtained.

image 1 Cardiovascular Curveball #006

Click to enlarge

Q1. Describe the ECG findings. What investigation is indicated?

The most significant finding on this ECG is the presence of electrical alternans. The rhythm is sinus tachycardia at 100bpm and the axis is normal. The investigation indicated is an echocardiogram to confirm the presence of a pericardial effusion and to exclude pericardial tamponade.

—

Q2. You ring the cardiologist to arrange the investigation in question urgently and he asks you to assess the degree of pulsus paradoxus. What is pulsus paradoxus and what are the potential causes of this phenomenon?

Pulsus paradoxus is defined as an inspiratory drop of 10mmHg or more during normal breathing. It is caused by:

1. pericardial tamponade
2. hypovolaemia
3. acute asthma
4. massive pulmonary embolism

On the cardiologist’s advice you assess the degree of pulsus paradoxus and no significant respiratory variation in systolic pressure is present.

—

Q3. You run into difficulty getting the investigation you have requested in a timely fashion because the cardiologist argues that the absence of pulsus paradoxus is reassuring. Is he right?

In this particular case, no.

Electrical alternans is usually associated with tamponade and there are many reasons why pulsus paradoxus may be absent in the presence of cardiac tamponade including:

1. pericardial adhesions (particularly over the right heart)
— impede volume changes

2. severe left ventricular failure or marked left ventricular hypertrophy
— in these circumstances the pericardial pressure effectively equilibrates only with the right heart pressures with the much less compliant left ventricle resisting phasically changing pericardial pressure

3. right ventricular hypertrophy without pulmonary hypertension
— causes right-sided resistance to the effects of breathing

4. atrial septal defects
— increased venous return balanced by shunting to the left atrium

5. severe aortic regurgitation
— produces sufficient regurgitant flow to damp down respiratory fluctuations

—

References and Links

Filed Under ECG Tagged With ECG, electrical alternans, lung cancer, pericardial tamponade

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

Metabolic Muddle #005

March 10, 2010 By Paul Young 4 Comments

A 20 year old male presents with 3 days of lethargy and generalised malaise.  He is confused and looks very unwell.  The following blood tests are obtained:

image 11b Metabolic Muddle #005

Click on image to enlarge

Questions

Q1. Describe the acid base disturbance.

There is a severe metabolic acidosis with a raised anion gap with an appropriate degree of respiratory compensation.

—

Q2. What is the likely diagnosis?

Diabetic ketoacidosis

—

Q3. Describe the electrolyte abnormalities.

The patient has hypernatraemia and, in fact, is even more hypernatraemic than is immediately apparent. The glucose is very high and, therefore, a correction is required.

The calculation is:

[Na+] + (glucose -10)/3

In other words, the corrected sodium is 166.

The potassium is very low.  This is particularly noteworthy given the degree of acidaemia.  Acidaemia drives the potassium up so, as the acid base disturbance is corrected, the potassium will drop even further.  While total potassium deficits can be difficult to predict on the basis of serum potassium, the  total loss here is likely to be in the order of 100s mmols.

The magnesium is not low which would be unheard of in this setting unless the patient had received magnesium supplementation (which they had).

The phosphate is low – this too is a common electrolyte disturbance in DKA.  There is debate about the significance of low phosphate in this setting but Intensivists (myself included) can’t resist correcting the phosphate.

—

Q4.Should the corrected sodium be used for calculating the anion gap?

No. The anion gap reflects the balance between positively and negatively charged electrolytes in the extracellular fluid. Glucose is electrically neutral and does not directly alter the anion gap. However, glucose is osmotically active so water is pulled into the extracellular fluid. This has a dilutional effect on all extracellular electrolyte concenations, both positive or negative, and so the anion gap is minimally altered.

—

Q5. It emerges that the patient has recently been diagnosis with Schizophrenia and has commenced olanzepine. What is the significance of this additional history?

There are some data that suggest an increased risk of diabetes and diabetic ketoacidosis in patients commenced on atypical antipsychotics.

—

Q5. An amylase is measured and is found to be 3 times the upper limit of normal. What is the significance of this finding?

Mild elevations in amylase are common in diabetic ketoacidosis and in the absence of other manifestations suggestive of pancreatitis are not of clinical significance.

—

References and Links

  • Beck, LH. Should the actual or the corrected serum sodium be used to calculate the anion gap in diabetic ketoacidosis? CLEVELAND CLINIC JOURNAL OF MEDICINE  2001; 68 (8) 673-674. (pdf)
Filed Under Blood Results, Clinical Case Tagged With antipsychotic induced ketoacidosis, arterial blood gas, data interpretation, DKA, ketaacidosis

UCEM Announces Electropenogram

February 24, 2010 By Peter Allely 11 Comments

The Utopian College of Emergency for Medicine (UCEM) is pleased to announce the introduction of a new diagnostic tool – the Electropenogram (EPG).

Professor Throckmorton, our new Head of the Committee Of Continuing Knowledge, has spent the last 13 years investigating Wolkenkuckucksheim and ithyphallic activity occuring in Electrocardiographs.

After an exhausting 12 month statistical analysis by the backroom boffins, the retrospective review of 26 832 ED cardiac tracings has finally been completed. The results of this BACCHUS-II trial are open to interpretation, lack little scientific credibility and are on the whole inaccurate. However, in this world of eminence based medicine where the statistics never lie it is prudent to take note of the studies findings.

  • Resting Positive Electropenograms were recorded in 2.6% of the general population, 3.4% of inmates and 13% of administrators (p = 0.02; 95% confidence interval, 1-99%)
  • The maximum prevalence of Positive Electropenograms occurred on Friday and Saturday evenings (80%) with a staggerring 93% on Public Holidays.

As yet it is uncertain as to what a positive Electropenogram might mean for the patient but some of the LITFL team have their theories…

ECG penis 600x600 UCEM Announces Electropenogram

EPG positive

Filed Under Cardiology, ECG, Emergency Medicine, Medical Humor, UCEM Tagged With ECG, EKG, electrocardiogram, electrokardiogram, Electropenogram, Emergency Medicine, humour, Medical Humor, throckmorton, UCEM

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

Sternoclavicular Joint Dislocation

February 6, 2010 By sandnsurf 18 Comments

Sternoclavicular joint dislocation is a relatively uncommon injury that can be easily missed or misdiagnosed. Bilateral posterior sternoclavicular joint dislocation is even rarer still…

The importance in determining the direction of dislocation is emphasised by the dichotomy of management. Hence, a thorough history and examination, especially looking for evidence of compression of retrosternal structures, is paramount. Specialised sternoclavicular X-ray views should be supplemented by CT/MRI if clinical suspicion is high. Posterior dislocations necessitate prompt orthopedic referral.

Case Report

A 30 year old man presented to ED with bilateral “shoulder pain” after a quad bike accident. Having taken a corner at high speed, he feel from the bike landing on his right shoulder and was crushed by the bike landing on his left shoulder.

On presentation, ABCs were intact. No dysphonia, dysphagia or dyspnoea.

Both right and left shoulders were dislocated anteriorly and were relocated at triage.

There was swelling and tenderness over both sternoclavicular joints and the patient was unable to abduct either shoulder actively despite glenohumeral enlocation. Passive movement of the shoulders was limited by pain “over the collarbone”, although the clavicles themselves were only tender near their junction with the sternum. Specifically, the AC joints and humerus were non-tender and arm neurovascular status was normal.

Initial Chest X-ray was performed and reported as normal

SternoClavicular Dislocation 001 s Sternoclavicular Joint Dislocation

However in light of the high clinical suspicion for sternoclavicular joint injury; continued anterior chest pain and failure in shoulder abduction special plain film tomography views of both SC joints was performed:

Sternoclavicualr Dislocation 002 s Sternoclavicular Joint Dislocation

There is widening of the right sternoclavicular joint when compared to the left side.  This appearance is suspicious for subluxation/dislocation. There is probable subtle widening of the left sternoclavicular joint as well. Several well-corticated bone ossicles are noted in the vicinity of the sternoclavicular joints bilaterally.

This was confirmed on CT scan:

Watch the 3D Video of the CT here

Sternoclavicular Dislocation 003 s Sternoclavicular Joint Dislocation

Superior dislocation of bilateral sternoclavicular joints. Associated fracture of the left 1st rib anteriorly noted.

Anatomy of the sternoclavicular joint

  • The sternoclavicular joint is a diarthodial saddle-type joint which provides a pivot for the shoulder girdle on the trunk.
  • The joint capsule is reinforced anterioposteriorly by the anterior and posterior sternoclavicular ligaments.  Superomedially the joint is reinforced by the interclavicular ligament which joins both the upper boarder of both clavicles to the suprasternal notch.
  • The clavicle is also bound to the first costal cartilage and the first rib by the costoclavicular ligament.

SCJ Dislocation Sternoclavicular Joint Dislocation

Original Description

Astley Paston Cooper Sternoclavicular Joint Dislocation

Sir Astley Paston Cooper

Sir Astley Paston Cooper (23 Aug 1768 – 12 Feb 1841)

An English surgeon and pioneer in experimental surgery. He was the first to tie the abdominal aorta in treating an aneurysm (1817), among various other operations he performed successfully at a time before antiseptic procedures. He was devoted to the study and teaching of anatomy, and is said to have dissected daily throughout his career.

In 1820 he excised and infected sebaceous cyst from the scalp of King George IV. He was appointed sergeant surgeon to George IV, William IV and Queen Victoria. He was elected President of the Royal College of Surgeons on two occasions (1827 &1836).

Sir Astley Cooper is credited with the first report of this entity in ‘A treatise on dislocations and on fractures of the joints‘ in 1824. Approximately 120 cases of posterior sternoclavicular joint (SCJ) dislocation have been documented in the medical literature since it was first described, a statistic which underlies its relative rarity.  Despite this statistic, emergency physicians should be familiar with the condition the mechanism of injury and physical findings and the potentially life-threatening injuries.

Clinical Presentation

Incidence

  • Sternoclavicular dislocations account for 3% of all shoulder girdle injuries.
  • 95% of SCJ dislocations are unilateral and anterior dislocations are far more common than posterior dislocations due to the weaker anterior sternoclavicular ligament (ratio 9:1). Bilateral superior dislocations, as in the case above, are rarely described.

Mechanism of Injury

  • Dislocations of the SCJ generally occur following a fall on the outstretched hand or a direct blow to the shoulder. Sporting injuries and motor vehicle accidents account for the most causes of SCJ dysfunction. However, they can also occur without any history of injury.
  • Patients commonly present with pain and swelling in the proximal sternum and sternoclavicular region. The pain will be exacerbated by lateral shoulder compression, arm movements, deep breathing or coughing.
  • Patients often laterally flex their neck towards the affected side to relieving pressure on the SCJ. Asymmetry is best appreciated when viewed from above the patient’s head.
  • Additional symptoms include dysphonia, dysphagia or dyspnoea.

Diagnostic Imaging

  • Plain X-ray: standard views may not provide a definitive diagnosis. Alternate views such as ’serendipity view’ (40-degree cephalic tilt) may provide more information.
  • CTA or MRA to determine direction of dislocation and potential for vascular compromise. A contrast study is required for definitive evaluation of surrounding structures.

Complications

Many complications have been reported in the literature related to retrosternal (posterior) dislocation of the medial end of the clavicle including:

Management

Simple sprain of the SCJ

  • Patients will complain of mild to moderate pain and there will be no joint instability on clinical examination.
  • Conservative treatment with ice, analgesia, shoulder sling for immobility will lead to complete recovery in 1 week.
  • Subluxation of the SCJ will require the application of a clavicular splint or sling for 3 to 6 weeks

Anterior SCJ Dislocations

  • Anterior sternoclavicular dislocations are usually managed nonoperatively.
  • The clavicle often stabilises in its subluxed position, with asymmetrical ventral protrusion of the affected side. The arm should be rested in a sling which will assist in the reduction of pain. Patients generally experience a good pain-free functional outcome at 2-3 weeks. Very rare complications include chronic pain, periarticular calcifications with ankylosis and progressive deformity.
  • Closed reduction may be indicated in rare circumstances where the patient is engaged in strenuous upper limb activities causing a painful SCJ. It is however, often unsuccessful. The application of direct pressure over the medial end of the clavicle may also reduce the joint.

Posterior SCJ Dislocations

  • Posterior sternoclavicular dislocations should always be reduced in theatre because of the associated risk to intrathoracic and superior mediastinal structures.

Example of a Unilateral Posterior Sternoclavicular Dislocation

Unilateral Posterior Sternoclavicular Dislocation

Unilateral Posterior Sternoclavicular Dislocation

Unilateral Posterior Sternoclavicular Dislocation

Unilateral Posterior Sternoclavicular Dislocation CT


Methods of reduction

The initial treatment of choice is a closed reduction. Various methods have been described:

  • Classical:  Patient positioned supine with a towel/sandbag between scapulae. Sedation is administered and traction is applied to the abducted arm with simultaneous extension. This has an 80% success rate.
  • Buckerfield and Castle: While shoulders are pushed posteriorly by an assistant, the ipsilateral arm is adducted against the torso and caudal traction is applied.
  • Towel Clip: Anterior traction force can be applied to clavicle by percutaneously applied towel clip, often used with one of the above methods.
  • A figure of eight sling is applied after the reduction for 4-6 weeks to allow for ligamentous healing.

If the SCJ becomes chronically unstable or if closed reduction is unsuccessful, then open reduction is indicated.

Discussion

Traumatic sternoclavicular joint dislocation is an uncommon condition whose diagnosis is often missed. The importance in determining the direction of dislocation is emphasised by the dichotomy of management. The posterior version of this dislocation has been associated with multiple complications and owing to the rarity of this injury, there is a relative lack of familiarity with the diagnosis, surgical anatomy and treatment options. [Reference]

A thorough history and examination, especially looking for evidence of compression of retrosternal structures, is paramount. Specialised sternoclavicular X-ray views should be supplemented by CT/MRI if clinical suspicion is high. Posterior dislocations necessitate prompt orthopedic referral.

References

ResearchBlogging.orgSaltzman, M., Mercer, D., Bertelsen, A., Warme, W., & Matsen, III, F. (2009). Bilateral posterior sternoclavicular dislocations Radiology Case Reports, 4 (1) DOI: 10.2484/rcr.v4i1.256

  • Jacques B. Jougon, MD, Denis J. Lepront, MD, Claire E. H. Dromer, M. Posterior Dislocation of the Sternoclavicular Joint Leading to Mediastinal Compression. [Reference]
  • Hoekzema N. Torchia M. Adkins M Cassivi SD. Posterior sternoclavicular joint dislocation [Reference]
  • Mirza AH, Alam K, Ali A Posterior sternoclavicular dislocation in a rugby player as a cause of silent vascular compromise: a case report. Br J Sports Med. 2005 May;39(5):e28. [Reference]
  • Asplund C, Pollard ME. Posterior sternoclavicular joint dislocation in a wrestler. Mil Med. 2004 Feb;169(2):134-6. [Reference]
  • Wirth MA, Rockwood CA Jr. Acute and Chronic Traumatic Injuries of the Sternoclavicular Joint.J Am Acad Orthop Surg. 1996 Oct;4(5):268-278. [Reference]
  • Brinker MR, Bartz RL, Reardon PR, Reardon MJ. A method for open reduction and internal fixation of the unstable posterior sternoclavicular joint dislocation. J Orthop Trauma. 1997 Jul;11(5):378-81. [Reference]
  • Saltzman, M., Mercer, D., Bertelsen, A., Warme, W., & Matsen, III, F. (2009). Bilateral posterior sternoclavicular dislocations Radiology Case Reports, 4 (1) DOI: 10.2484/rcr.v4i1.256
  • O’Connor PA. Nölke L. O’Donnell A. Maha Lingham A. Retrosternal dislocation of the clavicle associated with a traumatic pneumothorax [Reference]
  • Cooper A. A treatise on dislocations and on fractures of the joints. In: Longman, Hurst, Orme, Brown, Green, eds. London, 1824:359

An old Scotch physician, for whom I had a great respect, and whom I frequently met professionally in the city, used to say, as we were entering the patient’s room together, ‘Weel, Mister Cooper, we ha’ only twa things to keep in meend, and they’ll searve us for here and herea’ter; one is always to have the fear of the Laird before our ees; that ‘ill do for herea’ter; and t’other is to keep your booels open, and that will do for here.’ – Sir Astley Cooper

Research Credit – Dr Andrew Toffoli

Filed Under CT scan, Chest X-Ray, Featured, Investigation [tests], Medical Specialty, Orthopedics Tagged With Anatomy, clavicle, dislocation, joint, joint diclocation, posterior, SCJD, sternoclavicular

Oncology Quandary #004

February 3, 2010 By Paul Young 5 Comments

45 year old woman with metastatic ovarian cancer is admitted for VATS pleurodesis (video-assisted thoracoscopic surgery) and drainage of bilateral pleural effusions.  Her admission chest X-ray is shown below:

image 1 Oncology Quandary #004

During her operation, 2L of fluid is drained from the left chest.  Shortly thereafter, pink frothy sputum starts coming out of the ET tube and the patient markedly desaturates.  The patient is transferred to the intensive care unit and the following chest x-ray is obtained:

image 21 Oncology Quandary #004

Questions

Q1. Describe the chest X-ray.

There is an ET tube, a right IJ central line and bilateral chest drains in situ. There is also ECG monitoring on the patient. Most importantly:

There is near white-out of the left hemi-thorax.

—

Q2. What is the likely diagnosis?

The history and chest X-ray appearances suggest that the likely diagnosis:

re-expansion pulmonary oedema

Q3. What are the risk factors for this condition developing?

Risk factors include:

  1. long-standing collapse of the lung prior to aspiration
  2. drainage of a large amount of fluid or air over a short period of time
  3. application of suction

—

Q4. What is Meig’s syndrome?

Meig’s syndrome is the triad of:

  1. ascites,
  2. pleural effusion and
  3. benign ovarian tumor (fibroma)

It resolves after the resection of the tumor. For reasons unknown, the pleural effusion is classically on the right side. This patient has metastatic ovarian cancer with associated pleural effusion so this is not it!

Joe Vincent Meigs, was an American obstetrician and gynaecologist. Meigs was a grandson of Captain Joe Vincent Meigs, who invented an experimental steam monorail known as the Meigs single-track elevated railroad.

image 3 Oncology Quandary #004

Filed Under Chest X-Ray, Clinical Case, Education, Investigation [tests], Medical Specialty, Oncology, Respiratory Tagged With Chest X-Ray, Meigs syndrome, ovarian cancer, Re-expansion pulmonary oedema, unilateral white-out

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

Gastrointestinal Gutwrencher #001

February 1, 2010 By Chris Nickson 6 Comments

A 50 year-old man presented to the ED with sharp abdominal pain localised to his left lower quadrant.

The pain came on rapidly the day before, when he took his dog for a walk after dinner. The pain is non-radiating and worse on movement, but he has no other symptoms. Past medical history is unremarkable. His vitals were within normal limits, his abdomen was soft with no herniae or scrotal abnormalities, but he was distinctly tender in the left lower quadrant.

FBC, UEC and urinalysis were within normal limits. Following a surgical review, a CRP was ordered and the following CT abdomen was obtained:

GI gutwrencher #001

From Sand et al. (2007) – click to enlarge

Q1. What is the diagnosis?

Epiploic appendagitis

—

Q2. How common is this condition?

The diagnosis is rare.

This is partly because of low awareness of its existence among clinicians.

It can affect any age (mean ~45 years) and has a male preponderance. It is unclear if it is more common in the obese.
—

Q3. What causes this condition?

Epiploic appendages are the 50–100 fatty blobs that originate in two rows (anterior and posterior) either side of the taenia coli. They are 0.5 to 5 cm long and each is accompanied by one or two arterioles and a venule.

They may become inflamed as a result of torsion or spontaneous venous thrombosis.

Epiploic appendagitis most commonly affects the sigmoid, but also occurs in the cecum and other regions of the colon. However, patients with long sigmoids can have right-sided rather than left-sided pain.
—

Q4. What are the clinical features of this condition?

Abdominal pain and tenderness with the following characteristics:

  • More commonly LLQ than RLQ
  • localized, strong, non-migratory, sharp pain
  • usually starts after physical movement e.g. postprandial exercise

There is a lack of systemic features (e.g. fever, vomiting or leukocytic response), although CRP may be elevated.
—

Q5. What is the best way to make the diagnosis?

CT abdomen is the most reliable way of making the diagnosis, short of laparoscopic exploration. Epiploic appendages are not usually seen on CT due to fat attenuation, unless they are surrounded by intraperitoneal fluid or inflammation.

The pathognomonic CT scan finding  for epiploic appendagitis is the presence of a 2–4 cm, oval shaped, fat density lesion, surrounded by inflammatory changes.

The key features are:

  • Central focal area of hyper-attenuation with surrounding inflammation
  • ± Thickening of the parietal peritoneum wall
  • Diameter of the colonic wall is mostly regular without signs of thickening (unlike diverticulitis)

Epiploic appendagitis can be diagnosed on ultrasound but this modality has low sensitivity.

Investigations are generally targeted at excluding the serious conditions that epiploic appendagitis may mimic – especially appendicitis and diverticulitis.

—

Q6. How should this patient be managed?

This is somewhat controversial.

Epiploic appendagitis is generally considered a benign and self-limiting condition. Patients recover in <10 days and usually require only oral analgesia (e.g. paracetamol, NSAIDs)

However, the rate of recurrence – with pain localised to the same region – may be up to 40%. Some authorities suggest that surgical intervention may decrease this. The suggested approach is surgical exploration using laparoscopy, with simple ligation and excision of the inflamed appendage.
—

Reference

ResearchBlogging.org

  • Sand, M., Gelos, M., Bechara, F., Sand, D., Wiese, T., Steinstraesser, L., & Mann, B. (2007). Epiploic appendagitis – clinical characteristics of an uncommon surgical diagnosis. BMC Surgery, 7:11 DOI: 10.1186/1471-2482-7-11
Filed Under CT scan, Clinical Case, Emergency Medicine, Featured, Gastroenterology, General Surgery Tagged With abdominal pain, CT scan, epiploic appendagitis

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

Radiological Oddity #019

January 25, 2010 By sandnsurf 3 Comments

MS0980469.11 590x679 Radiological Oddity #019

MS0980469.37 590x373 Radiological Oddity #019

MS0980469.28 Radiological Oddity #019

Filed Under CT scan, General Surgery, Investigation [tests], Medical Specialty, X-Ray Tagged With AXR, CT, USS

Metabolic Muddle #003

January 15, 2010 By Paul Young 6 Comments

An 87 year old female presented with a subarachnoid haemorrhage.  GCS 8/15.  A nasogastric tube was unable to be placed due to patient agitation.  As a consequence, the patient was fasted for five days due to concern about swallowing.   Subsequently, an arterial blood gas was obtained:

image 14 Metabolic Muddle #003

Questions

Q1. Describe the arterial blood gas

  1. There is a metabolic acidosis with a high anion gap (HAGMA).
  2. The bicarbonate has decreased by more than the anion gap has increased which is due to a coexistent normal anion gap acidosis (NAGMA).
  3. There is a respiratory alkalosis. The pCO2 of 12mmHg is much lower than the respiratory compensation you would expect with this degree of metabolic acidosis (expected pCO2 = 1.5 * HCO3 +8 = 25 ).

The combination of these three abnormalities has led to relatively normal pH despite severe acid-base disturbance.

—

Q2. What are the causes of metabolic acidosis with raised anion gap and what is the likely cause here?

There are two ways of remembering this.

The easy way is to remember ‘left total knee replacement’:

Lactate
Toxins
Ketones
Renal Failure

The more complicated way is CAT-MUDPILES:

Cyanide, Carbon monoxide
Alcoholic ketoacidosis
Toluene
Methanol, metformin
Uraemia
Diabetic Ketoacidosis
Phenformin, pyroglutamic acidosis, propylene glycol, paracetamol
Isoniazid, Iron
Lactic acidosis (many causes)
Ethanol, Ethylene glycol
Starvation, salicylates

The history suggests starvation ketoacidosis. There were ketones in the urine confirming this diagnosis.

Q3. What are the causes of normal anion gap acidosis and what is the likely cause here?

The easy way to remember is OGRe:image 24 Metabolic Muddle #003

Others (eg chloride)
GI loss
Renal loss

The more difficult way is to remember is USED CARP (the A and the R can be reversed – this is optional):

Ureteroenterostomy
Small bowel fistula
Extra Chloride
Diarrhoea
Carbonic anhydase inhibitors
Addisons disease
Renal tubular acidosis
Pancreatic fistula

Neurosurgeons like to give everyone lots of normal saline. The chloride is high. The likely diagnosis is hyperchloraemic metabolic acidosis secondary to normal saline.

Filed Under Blood Results, Clinical Case Tagged With arterial blood gases, metabolic acidosis, triple acid base disturbance

ENT Equivocation #001

January 13, 2010 By Paul Young 10 Comments

A 38 year old male with a background history of type 2 diabetes presents with fevers, rigors and pain on swallowing. There is no sign of impending airway compromise; however, marked trismus is noted. The following plain X-ray is obtained:

image 13 ENT Equivocation #001

Questions

Q1. What is the diagnosis?

there is gross soft tissue swelling evident anterior to the vertebral bodies. The likely diagnosis is retropharngeal abscess

Q2. What radiological investigation is indicated now?

A CT neck will allow you to determine the extent of the collection and whether it is amenable to drainage

image 21 ENT Equivocation #001

Q3. Describe the CT scan

There is an area of hypodensity in the right posterior pharynx consistent with an abscess.

Q4. The chest X-ray is normal but the ENT surgeon requests a CT chest. What do you think the purpose of this investigation is?

A CT chest is indicated to exclude unappreciated mediastinal mischief due to descending mediastinitis. This is a rare but highly lethal complication.

Q5. What is Lemierre’s syndrome?

Lemierre’s syndrome is characterised by disseminated abscesses and thrombophlebitis of the internal jugular vein after infection of the oropharynx. The predominant pathogen is a gram-negative anaerobic bacillus, Fusobacterium necrophorum.

Filed Under CT scan, Investigation [tests], X-Ray Tagged With ENT, retropharyngeal abscess

Hyperkalaemia

January 12, 2010 By Kane Guthrie 18 Comments

Case Study of Hyperkalemia:

George is a 72 year old male found collapsed at home on floor of his bedroom, incontinent of urine and faeces. He complained of significant pain in his right hip with shortening and rotation. George’s family last had contact with George 3 days prior to his collapse.

Assessment:

  • On arrival at ED he is confused and combative with a GCS 0f 13
  • Initial observations reveal BP 78/60; Pulse 74, RR 32, SPO2 91% (NRB 15L)
  • ABG which shows a Potassium of 9.0, pH of 7.23 and a Blood Glucose Level of 32mmol

Paste Medical History:

  • CCF
  • Hypertension
  • Type 2 DM
  • Osteoarthritis

Medication History:

  • George is taking  enlapril for hypertension; spironolactone & metoprolol for his CCF and celebrex for his osteoarthritis
  • His diabetes is diet controlled.

An ECG is performed on his arrival to the resuscitation area…

Hyperkalaemia ECG

You briefly review the ECG and confidently state (already knowing the ABG result) that this patient has sever hyperkalemia. Brilliant…now what?

The 5 C’s of Metabolic Disturbances

I use the 5 C’s approach to recognise, understand and manage metabolic disturbances in the ED.

  • Causes - Understanding normal metabolic homeostatic mechanisms helps define potential causative events that lead to disruption of the sensitive pathophysiological milieu. Increased production; increased intake and decreased excretion are often the commonest causal factors in metabolic disruption.
  • Clinical manifestations – evaluate, recognise and diagnose the problem
  • Complications – what can go wrong in the short, medium and long term can define clinical manifestation, duration of illness and potentially affect management decisions
  • Calculations – Calculate to Obviate
  • Corrective measures – Call to action…how do you actually fix the problem!

Potassium Pathophysiology

  • Serum potassium is normally maintained between 3.5 -5.0 mmol/L
  • Hyperkalaemia is defined as a potassium level greater than 5.5 mmol/L
  • Hyperkalaemia is a potentially life-threatening metabolic problem caused by inability of the kidneys to excrete potas­sium, impairment of the mechanisms that move potassium from the circulation into the cells, or a combination of these factors.

Classic Causes of Hyperkalaemia

  • Excessive exogenous potassium load (Increased Intake)
    • Potassium supplements (IV or Oral)
    • Excess in diet
    • Salt substitutes (e.g. potassium salts of penicillin)
  • Excessive endogenous potassium load (Increased Production)
    • Haemolysis
    • Rhabdomyolysis
    • Extensive burns
    • Tumor Lysis Syndrome
    • Intense physical activity
    • Trauma (especially crush injuries and ischaemia)
  • Redistribution (Shift from intracellular to extracellular fluid)
    • Acidosis (metabolic or respiratory)
    • Insulin deficiency
    • Drugs
      • Succinylcholine
      • Beta-blockers
      • Digoxin (acute intoxication or overdose)
    • Hyperkalemic familial periodic paralysis
  • Diminished potassium excretion (Decreased Excretion)
    • Decreased glomerular filtration rate (eg, acute or end-stage chronic renal failure)
    • Decreased mineral corticoid activity
    • Defect in tubular secretion (eg, renal tubular acidosis II and IV)
    • Drugs (eg, NSAIDs, cyclosporine, potassium-sparing diuretics, ACE Inhibitors)
  • Pseudohyperkalemia (Factitious)
    • Haemolysis (in laboratory tube) most common
    • Thrombocytosis
    • Leukocytosis
    • Venepuncture technique (e.g. prolonged tourniquet application)

Clinical Manifestations

Signs and Symptoms of Hyperkalaemia:

  • Clinical features are often non specific
  • Generalised muscle weakness
  • Flaccid paralysis and parathesia of the hands and feet
  • Lethargy, Confusion, Weakness and Palpitations

ECG Changes of Hyperkalaemia:

  • The ECG is one of the most important diagnostic tools in detecting hyperkalaemia
  • Predicted ECG changes associated with Hyperkalaemia include
Serum Potassium (mmol/L) Predicted ECG status
5.5-6.5 Tall tented T waves
6.5-7.5 Loss of P wave
7.5-8.5 Widening QRS
>8.5 QRS continues to widen, approaching to sine wave

ECG Changes of Hyperkalaemia:

ECG Hyperkalemia Changes1 Hyperkalaemia

Early ECG changes showing Peaked T waves

ECG Hyperkalaemia 7.1 s Hyperkalaemia

ECG Potassium 7.1

ECG of patient with Potassium of 8.5 mmol/L

hyperkalaemia

ECG Potassium 8.5

Potassium of 9.0mmol/L on 12 lead ECG.

Hyperkalaemia ECG

ECH Potassium K+ 9.0

Management of Hyperkalaemia

Treatment of hyperkalaemia involves stabilizing the myocardium to prevent arrhythmias, shifting potassium back into the intracellular space and removing excess potassium from the body.

1. Correct Serious Conduction Abnormalities (Calcium)

  • Calcium is a very useful agent. It does not lower the serum potassium level, but instead is used to stabilise the myocardium, as a temporising measure. Calcium is indicated if there is widening of QRS, sine wave pattern (when S and T waves merge together), or in hyperkalaemic cardiac arrest.
  • The ‘cardiac membrane stabilising effects’ take about 15-30mins.
  • Calcium Chloride
    • Dose: Calcium Chloride 10% 5-10mL
    • 3 x more potent than Calcium Gluconate
    • Complication: severe thrombophlebitis
  • Calcium Gluconate:
    • Dose: Calcium Gluconate 10% 5-10mL
    • Less potent, less irritating to veins
  • Potential Complications of Calcium administration
    • Bradycardia, hypotension and peripheral vasodilation
    • Generally these occur if administered too quickly
    • Avoid in digoxin toxicity (use magnesium as alternative)

2. Drive Potassium into the Cell:

  • Insulin & Glucose
    • Dose: IV fast acting insulin (actrapid) 10-20 units and glucose/dextrose 50g 25-50ml
    • Insulin drives potassium into cells and administering glucose prevents hypoglycaemia.
    • Begins to work in 20-30mins reduces potassium by 1mmol/L and ECG changes within the first hour
  • Sodium Bicarbonate
    • Dose: 50- 200mmol of 8.4% Sodium Bicarbonate
    • Bicarbonate is only effective at driving Potassium intracellullarly if the patient is acidotic
    • Begins working in 30-60 minutes and continues to work for several hours.
  • Salbutamol
    • Dose: 10-20mg via nebulizer
    • Beta 2 agonist therapy lower K via either IV or nebulizer route.
    • Salbutamol can lower potassium level 1mmol/L in about 30 minutes, and maintain it for up to 2 hours.
    • Very effective in renal patients that are fluid overloaded

3. Eliminate Potassium From the Body:

  • Calcium Resonium
    • Dose: 15-45g orally or rectally, mixed with sorbitol or lactulose
    • Calcium polystyrene sulfonate is a large insoluble molecule that binds potassium in the large intestine, where it is excreted in faeces
    • Effects take 2-3 hours
  • Frusemide
    • Dose: 20-80mg depending on hydration status
    • Potassium wasting diuretic. Helps to urinary excrete potassium in conjunction with hydration or fluid overloaded patients
  • Normal Saline
    • Used to help renally excrete potassium, by increasing renal perfusion and urinary output. Cautious use in patients with renal & heart failure
  • Dialysis
    • Is the gold standard for removing potassium from the body. Provides immediate and reliable removal.
    • Can lower potassium by 1mmol/L in first hour and another 1mmol/L over the next 2 hours.

References

  • Garth, D. (2009). Hyperkalemia. http://emedicine.medscape.com/article/766479-overview
  • Hall, B., Salazar, M., & Larison, D. (2009). The Sequencing of Medication Administration in the Management of Hyperkalaemia. Journal of Emergency Nursing, 35:4, 339-342.
  • Hollander-Rodriguez, J., & Calvert, J. (2006). Hyperkalemia. American Family Physician, 73:2, 283-290.
  • Pasco, J. (2009). Electrolyte Disturbances. In Cameron, P., Et al (Eds), Textbook of Adult Emergency Medicine (pp.447-507).China: Elsiever.

Hyperkalaemia even affects ED Consultants!!!

Carter Coding

embedded by Embedded Video

YouTube Direkt

Filed Under Cardiology, Clinical Case, Clinical Interpretation, ECG, Featured, lecture notes Tagged With hyperkaleamia, hyperkalemia

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

Elbow Dislocation

January 4, 2010 By sandnsurf 4 Comments

Elbow dislocations constitute 10% to 25% of all injuries to the elbow. The elbow is one of the most commonly dislocated joints in the body, with an average annual incidence of acute dislocation of 6 per 100,000 persons. Among injuries to the upper extremity, dislocation of the elbow is second only to dislocation of the shoulder.

Simple or Complex

Simple dislocations are described by the direction of the dislocated ulna. Posterior or posterolateral displacement of the ulna relative to the distal humerus is the most common simple dislocation with approximately 90% occurring this way (see image ). Rarer injuries include lateral and anterior displacements of the forearm.

When larger intra-articular fractures of the radial head, olecranon, or coronoid process occur with elbow dislocation, the injury is termed a complex dislocation.  Complex dislocations are much less common than simple dislocations. The risk of recurrent or chronic instability and posttraumatic arthrosis is increased significantly with complex dislocation.

Anterior Elbow Dislocation 590x438 Elbow Dislocation

AP and lateral Anterior Elbow Dislocation

Anatomy

The elbow joint  is one of the most inherently stable articulations. This stability is provided by the osseous and articular components with the shape and contour of the ulnohumeral articular surface providing anterior-posterior stability, varus/valgus, and rotatory stability. The capsuloligamentous components, which include the medial and lateral collateral ligaments and joint capsule, provide further stability by completing a structural ring about the elbow joint. Disruption of this ring is leads to elbow dislocation.

Elbow Ring 590x384 Elbow Dislocation

Finally the musculotendinous components, which include the muscles crossing the elbow joint, also contribute to the stability.

Lateral XR of Posterior Elbow Dislocation

Lateral XR of Posterior Elbow Dislocation

AP XR of Posterior Elbow Dislocation

AP XR of Posterior Elbow Dislocation

Evaluation

Patients present following a traumatic injury with swelling and deformity about the elbow. The mechanism of injury is usually a fall onto an outstretched hand.

TIP:  Elbow dislocation is sometimes confused with a supracondylar fracture. The two may be distinguished clinically by palpating for the equilateral triangle formed by the olecranon and epicondyles. This will be undisturbed in supracondylar fractures but distorted in elbow dislocations.

Neurovascular injury is uncommon, but should always be sought. Clinical evaluation should include median and ulna nerve function. Damage to the brachial artery can be assessed by palpating for a radial pulse.

After a complete examination, AP and lateral X-Rays of the elbow should be examined to determine the direction of the dislocation and to identify any associated fractures.

Evaluation of the Elbow dislocation

Clinical Evaluation of the Elbow dislocation

Management

Reduction can usually be carried out in the emergency department. It requires adequate muscular relaxation and appropriate analgesia. A fair amount of force is often required. Reduction may be achieved by correction of the medial or lateral displacement followed by strong traction on the forearm in the line of the limb. The arm may enlocate at this stage with a characteristic and satisfying reduction ‘clunk’. If not, firm pressure is applied posteriorly to the olecranon to bring it distally and anteriorly around the humeral trochlea. Traction should be maintained with the arm in moderate flexion, using counter-traction with the fingers. (see fig) Again a palpable ‘clunk’ will confirm reduction. Palpation should ensure the equilateral triangle formed by the olecranon and epicondyles is present.

TIP: After reduction, the elbow should be taken through a range of motion to evaluate joint stability. The elbow should be slowly extended and the angle at which tendency to redislocation occurs should be recorded. Most dislocated elbows are unstable to valgus stress (best tested in pronation to lock the lateral side).

Elbow relocation 1 Elbow Dislocation

X-Rays should then be performed in two planes, AP and lateral to ensure the reduction is concentric. Widening of the joint space may indicate entrapped osteochondral fragments. These patients should be referred to Orthopaedics for surgical debridement.

Note: Although X-Rays reveal periarticular fractures in 12% to 60% of cases, surgical exploration documents unrecognized osteochondral injuries in nearly 100% of acute elbow dislocations. Fortunately, the vast majority do not require operative intervention.

If the reduction is concentric and the joint is stable, the elbow should be splinted in 90 degrees of flexion. Patients should be followed up in 3-5 days with repeat X-rays to check reduction.

Enlocation 590x442 Elbow Dislocation

Complex dislocations

Complex elbow dislocation consists of both ligamentous and bony injuries. When one of the osseous or articular component structures of the elbow is disrupted, the risk of recurrent instability and arthrosis is greatly increased. Early mobilization of simple dislocations after closed reduction is associated with low risk of redislocation. These injuries, are more difficult to treat, and often have poorer results than simple dislocation. Fortunately they are much less frequent.

The radial head and coronoid process are the most commonly fractured structures in these injuries. Other structures that can be damaged include: medial and lateral collateral ligaments; medial and lateral condyles/epicondyles; transolecranon fractures and; posterior Monteggia fractures.

This disrupts the structural ring which provides stability to the elbow joint (see figure above). If there is evidence of disruption of one component of the ring, a second disruption is likely.

Note: The terrible triad consists of dislocation with associated radial head and coronoid process fracture.

Complex dislocations should have the same initial treatment- with clinical evaluation and reduction- as simple dislocations. They should all be referred to the inpatient Orthopaedic Surgery team for ongoing management, as they will require surgical repair.

Author Credit: Dr W G Blakeney

Filed Under Education, Featured, Investigation [tests], Medical Specialty, Orthopedics, X-Ray, eLearning Tagged With dislocation, Elbow, Elbow dislocation, eLearning, orthopaedics

Renal Riddle #001

December 29, 2009 By Paul Young 10 Comments

Consider a 65 year-old male presenting with right-sided flank pain radiating to the groin.  The following CT scan was taken to confirm a presumed diagnosis of renal colic:

image 114 Renal Riddle #001

image 210 Renal Riddle #001

Questions

Q1.  Describe the CT scan

CT scan is non-contrast; however, there is:

  • right-sided retroperitoneal blood evident.
  • an abdominal aortic aneurysm.

It is important to remember that the commonest cause of the ‘classic’ presentation of renal colic amongst patients presenting to have a post-mortem is ruptured abdominal aortic aneurysm.

This patient needs an emergency AAA repair.

The patient was taken to theatre for emergency surgery.
The following biochemistry results were taken post-operatively:

image 37 Renal Riddle #001

Q2.  Describe the biochemistry.  What diagnosis is suggested by these biochemical findings?

Biochemistry demonstrates acute renal failure with a reduced urea-to-creatinine ratio.

The likely diagnosis is rhabomyolysis in this clinical context. Features suggestive of this diagnosis are:

  • increased urea and creatinine with a reduced urea-to-creatinine ratio
  • hyperphosphataemia, hypocalcaemia, hyperkalaemia
  • metabolic acidosis
  • increased CK (usually to greater than 40,000)
  • Although not measured here, AST, and LDH are also increased in rhabdomyolysis

Q3.  What are the other potential causes of renal failure to consider in this clinical situation?

  1. hypovolaemia from bleeding
  2. renal artery occlusion during operation
  3. use of contrast in pre-operative CT scan (not in this case)
  4. use of nephrotoxic drugs like gentamicin
  5. low cardiac output from peri-operative myocardial infarction
  6. abdominal compartment syndrome

Filed Under Blood Results, CT scan, Clinical Case Tagged With abdominal aortic aneurysm, renal colic, renal failure, rhabdomyolysis

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
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