Monday, November 13, 2017

The Crashing Patient Conference: A Must Go!

As I was putting together my slides for the ACEP 2017 Conference, I saw a tweet pop up. It was by Dr. Amal Mattu (@amalmattu) advertising about The Crashing PatientConference in Baltimore in October 2017. It was the very same month I was going to Washington DC for my one month of clinical rotation at George Washington University Hospital. I was super-excited! It became a top priority to register myself for the conference. I was dreaming of meeting my Emergency Medicine gurus in person and this was an excellent opportunity, which I could hardly lose.

The Crashing Patient Conference is an annual one da conference which has many short lectures with ‘to the point’ pearls. This year’s theme was resuscitation and risk management. There were different lectures encompassing critical care, resuscitation, shock, cardiology, endocrine emergencies, orthopaedics, paediatrics, urology, burns and most importantly medico-legal.




I will summarize the pearls here from each session. Dr. Mike Winters reviewed critical care quickies with an interesting case that he had encountered.
1)     Before intubating the patient,  preoxygenate with 40-60L/min by NRBM
2)     RSI drugs: remember TBW for etomidate and IBW for ketamine (Obese patients were found to be dosed inappropriately)
3)     ED ventilator settings matter, especially if there is increased length of stay in ED!
4)     Deep sedation is known to increase mortality. Target lighter level of sedation. Opioids (Fentanyl) are first line!

Dr. Khoujah talked about delirium, which is misdiagnosed most of the time.
1)     In patients with suspected delirium, pay attention to “attention”.
2)     Use modified Richmond Agitation and Sedation Scale to screen delirium.
3)     Delirium = predisposing condition + precipitating insult; treat the underlying cause
4)     Change the environment ie allow relatives to be besides the patient, put a date time and location on wall facing the patient, try to minimize physical restraints.
5)     Most importantly, prevent delirium before you have to treat it!

Dr. Manning discussed on ventilator settings in severe asthmatics.
1)     Stick to the basic asthma medications
2)     Maintain permissive hypercapnia by balancing acidosis and auto-PEEP
3)     Indication for intubation: cardiac arrest, exhaustion, agitation, silent chest and severe hypoxia
4)     Lower the respiratory rate, allow patient time to breathe. Reduce I:E ratio to 1:4.
5)     Increase tidal volume to 8-10ml/kg, lower the PEEP and increase the flow rate 80L/min and gradually taper FiO2.
6)     Trouble shooting : a)Post-intubation hypotension- disconnect from vent, let them exhale then check for pneumo. b) Post-intubation hypoxia- do the above and check the tube c) post-intubation arrest- ACLS, go easy on bagging, needle the chest
7)     When in doubt, disconnect and let the air out!

Dr. Bontempo discussed about deep neck space infection and things to remember.
1)     The most common etiology of deep neck space infection is odontogenic; specifically infections of lower 2nd and 3rd molars.
2)     One should be worried if voice change, shortness of breath, neck pain, DM, CRP >100
3)     Anticipate a difficult airway, start broad spectrum abx, drain the pus out.

Dr. Dubbs discussed about the law suits faced due to missed diagnosis of cancer in ED. She suggested:
1)     Always have a high index of suspicion- prolonged symptoms, weight loss, B symptoms, voice change, stool change, anorectal lesions, post-menopausal bleeding
2)     Watch out for the fine printed reports- incidental findings, abnormal cell counts, etc.
3)     Discuss with the patient
4)     Document your discussion and have a great QA process

Dr. Bond (@Docbond007) talked about spinal epidural abscess and posterior shoulder dislocation.
1)     The incidence of epidural abscess has increased in past 2 decades, keep a high suspicion for patients presenting with spine pain.
2)     In patients with spine pain without any neuro deficit, but with fever, risk factors, then check CRP/ESR; if elevated get an MRI spine.
3)     Get X-ray axillary view in suspected posterior shoulder dislocation. Ensure humeral head is in glenoid cavity.

Dr. Lu discussed the complications of myocarditis. It can be deadly in kids. Hence
1)     Always be wary of subtle signs
2)     Consider myocarditis if dyspnoea, chest discomfort and antecedent viral illness.
3)     Consider myocarditis if persistent unexplained tachycardia.

In the section on ‘Salt, sugar and sex’, Dr. Willis summarized that
1)     Persistently hypoglycemic- think adrenal insufficiency
2)     Hypoglycemia +hypotension – Adrenal insufficiency until proven otherwise
3)     If there is any suspicion give empiric steroids. (Hydrocortisone 100mg iv, Dexamethasone 5mg iv, fludrocortisone 0.1mg iv

During the conference, Dr. Mattu kept the audience engaged by his fun quiz. He was kind to gift me the signed copy of the second edition of ‘Avoiding common errors in Emergency Department’ which I will treasure the most.

Although it was a long day, but due to short engaging presentations in a TEDx like format, it was very fun filled, motivational and interesting conference. A definite must go!


Summary prepared by:

Nikhil N. Tambe - @nikhil16mar
M.B.B.S., ECFMG (USA)


Emergency Medicine Resident 
Masters in Emergency Medicine (GWU)
Kokilaben Dhirubhai Ambani Hospital, Mumbai
Instructor (American Heart Association)
Lifesupporters Institute of Health Sciences, Mumbai






Monday, November 6, 2017

Sternoclavicular joint Injuries

Sternoclavicular joint is an  extremely stable joint, due to the strong surrounding ligaments, and thus fracture/dislocations are rare and most injuries simple sprains. Significant forces are required to disrupt the strong ligamentous stabilizers of this joint. The most common causes are MVCs and injuries sustained in contact sports.
 The joint may be anteriorly or posteriorly dislocated.





Grading on Injury
Injuries to the SCJ can be graded into three types. A grade I injury is a mild sprain secondary to stretching of the sterno-clavicular and costoclavicular ligaments. A grade II injury is associated with subluxation of the joint (anterior or posterior) secondary to rupture of the sternoclavicular ligament. The costoclavicular ligament remains intact. Complete rupture of the sternoclavicular and costoclavicular ligaments results in a grade III injury (dislocation).

Minor trauma may result in a sprain are treated with with ice, sling, and analgesics and follow up with Orthopaedics. 

Anterior and Posterior Dislocation
Results from a direct blow to the shoulder, causing the shoulder to roll forward. Patients present with severe pain which is exacerbated by arm movement and lying supine. The pain will be exacerbated by lateral shoulder compression, arm movements, deep breathing or coughing.The shoulder may appear shortened and rolled forward. 


http://msk-anatomy.blogspot.co.uk/2012/06/sternoclavicular-joint.html

On examination, anterior dislocations have a prominent medial clavicle end that is visible and palpable anterior to the sternum while in posterior dislocations, the medial clavicle end is less visible and often not palpable, and the patient may have signs and symptoms of impingement of the superior mediastinal contents, such as stridor, dysphagia, and shortness of breath. 



Imaging
CXR is needed to exclude a injuries such as a  pneumothorax, pneumomediastinum, and hemopneumothorax. Routine radiographs have a low sensitivity for the detection of dislocation and thus special views and comparison with the other clavicle may be required. CT remains the imaging procedure of choice and is recommended especially in any posterior dislocation with concern for injury to the mediastinal structures. 



Management

Anterior Dislocation
Patients with uncomplicated anterior dislocations may be discharged without an attempted reduction. Look for concomitant Glenohumeral and Acromioclavicular joint injuries. Clavicular splinting, ice, analgesics, sling, and orthopedic referral are required.

Closed reduction may be performed within 10 days of the injury by placing the patient supine with a towel rollin between the shoulder blades. The arm is then abducted to 90 degrees and longitudinal traction is applied with slight extension by moving the arm toward the ground, and pressure is placed over the medial end of the clavicle. The application of direct pressure over the medial end of the clavicle may also reduce the joint. Post reduction, the patient should be placed in a figure of * brace for 4-6 weeks. Despite successful reduction, the joint is usually remains unstable and redislocates in half of the cases.




The use of acute reduction of anterior dislocations is controversial as most end up redislocating and reduction techniques risk injury to mediastinal structures.


Posterior Dislocation
Posterior dislocations may be associated with life-threatening injuries to adjacent structures, including pneumothorax or injury to surrounding great vessels, trachea, or oesophagus.  Orthopedic consultation is necessary for closed or open reduction. Open reduction should be performed in the operating room.


Take Home
  • Posterior dislocations necessitate prompt orthopaedic referral and looking for evidence of compression of retrosternal structures.
  • Anterior dislocations often remains unstable post treatment and thus acute reduction is debatable. 


Further Reading:
  • Rosen's Emergency Medicine - 7th Edition
  • TIntinalli's Emergency Medicine - 8th Edition
  • LIFTL
  • ALiEM
  • Morell, D. J., & Thyagarajan, D. S. (2016). Sternoclavicular joint dislocation and its management: A review of the literature. World Journal of Orthopedics, 7(4), 244–250. http://doi.org/10.5312/wjo.v7.i4.244

Posted by:

              
     Lakshay Chanana
     
     Speciality Doctor
     Northwick Park Hospital
     Department of Emergency Medicine
     England

     @EMDidactic




Monday, October 30, 2017

Thyroid Storm

Thyroid hormone exists in two forms: thyroxine and triiodothyronine. The ratio of thyroxine to triiodothyronine released in the blood is about 20:1 and peripherally, thyroxine is converted to the active triiodothyronine (T3), which is three to four times more potent than thyroxine.

Basic Terminologies
  • Primary hyperthyroidism is caused by the excess production of thyroid hormones from the thyroid glands. 
  • Secondary hyperthyroidism is caused by the excess production of thyroid-releasing hormones (Hypothalamus) or thyroid-stimulating hormones (Pituitary).

  • Hyperthyroidism refers to excess circulating hormone resulting only from thyroid gland hyper function. Most commonly cause by Graves' Disease. 
  • Thyrotoxicosis refers to excess circulating thyroid hormone originating from any cause. 
  • Thyroid storm is an extreme manifestation of thyrotoxicosis. It presents as an acute life-threatening hypermetabolic state caused either by excessive release of thyroid hormones or due to altered peripheral response to thyroid hormone following a precipitating event. 

Causes of Hyperthyroidism
  • Graves' Disease
  • Toxic Goitre
  • Thyroiditis (Viral, Radiation)
  • Hashimoto's
  • Secondary (Pituitary or Hypothalamus related)
  • Thyrotoxicosis Factitia
  • Drug Induced (Amiodarone, Interleukin 2)
  • Metastatic (Struma Ovarii)
  • Hydatidiform Mole

Precipitants of Thyroid Storm
  • Trauma
  • Heat related Illness
  • Recreational Drug Use
  • Psychosis
  • Stress
  • Infection
  • Iodinated Contrasts
  • ACS
  • DKA/HHS
  • Thyroxine Overdose
Consider thyroid Strom in any patient presenting with fear, tachycardia and altered mental status. Use Burch-Wartofsky scale to gauge your suspicion and diagnosis. 





Management
Following the order of treatment is of utmost importance here. Inhibition of thyroid gland synthesis of new thyroid hormone with a thionamide (Methimazole or PTU) must be initiated before iodine therapy.


1. Supportive care 
  • ABC
  • Cardiac Monitor and IV accsess.
  • Fluids, Maintenance of Electrolytes and Glucose. Cooling for hyperthermia. 
  • Add antibiotics as infection is a known precipitant and hard to distinguish in ED
  • Consider Cholestyramine to decrease the reabsorption of thyroid hormone from the enterohepatic circulation. In thyrotoxicosis, there is increased enterohepatic circulation of thyroid hormone. 

2. Inhibition of new hormone synthesis
Thionamides: Methimazole or PropylThioUracil. Thionamides decrease the synthesis of new hormone production. 

Methimazole: 40 to 100 milligrams PO as loading dose then 20 milligrams q4h


Propylthiouracil: Load with 600 to 1000 mg PO followed by 200 to 250 milligrams every 4 hours. PTU is hepatotoxic but in addition to decreasing the synthesis of new hormone production, it also blocks the peripheral conversion of thyroxine to triiodothyronine. 


Use PTU in first trimester and Methimazole in second and third trimester. 

 3. Inhibition of thyroid hormone release
Potassium iodide can be given to stop thyroid hormone release. PTU or Methimazole must be started first and Iodine therapy should be given at least 1 hour later. Iodine therapy blocks the release of pressured hormone. Start with 8 to 10 drops initially. 


Iodine-containing solutions should not be given to patients with iodine overload or iodine-induced hyperthyroidism or amiodarone-induced thyrotoxicosis. Lithium or potassium perchlorate should be used instead. 

 4. Peripheral β-adrenergic receptor blockade

Propranolol can be given IV in slow 1- to 2-milligram boluses q5-10min. Orally, propranolol therapy usually begins at 20 to 120 milligrams per dose.

 5. Preventing peripheral conversion of thyroxine to triiodothyronine 
The peripheral conversion of thyroxine to triiodothyronine is blocked by propylthiouracil, propranolol, and glucocorticoid. Glucocorticoids are essential in treatment since blockade produced by propylthiouracil and propranolol is not significant. . Glucocorticoid also treat underlying relative adrenal insufficiency. 

6. Find and treat the precipitation event (Sepsis, DKA, ACS)
7. Definitive Treatment - Radioactive Iodine or Surgery 



Other potential considerations:
  • Direct removal of thyroid hormone with plasma exchange
  • Use of Potassium Perchlorate in Amiodarone induced thyrotoxicosis: Potassium perchlorate  interferes with the production of new hormones 
  • Lithium: Used in cases of hypersensitivity to iodine. Lithium inhibits thyroid hormone release from thyroid gland. Typical dosing in thyroid storm is 300 milligrams every 8 hours. Monitor levels to avoid toxicity. 
  • Peripheral beta blockade: Reserpine or Guanethidine can be used, if there is a contraindication for BB use. These agents do not block beta receptors and interfere with catecholamine function (by depleting stores and blocking release)

Take Home:
  • Consider Thyroid Strom in any patient presenting with fever, tachycardia and Altered Mental Status.
  • PTU or Methimazole must be started first and Iodine therapy should be given at least 1 hour later.
  • Manage with beta blockers, PTU/Methimazole, Steroids and Potassium iodide
  • Identify and treat the precipitation cause 

Further Reading
Posted by:

              
     Lakshay Chanana
     
     Speciality Doctor
     Northwick Park Hospital
     Department of Emergency Medicine
     England

     @EMDidactic








Sunday, October 22, 2017

The patient with Long lie - Rhabdomyolysis

Skeletal muscle injury caused by any mechanism (direct, genetic, biochemical) is termed as rhabdomyolysis. Injured muscle fibers release cellular contents into the circulation leading to myoglobinuria. Besides myoglobin, cellular contents also include enzymes suck as creatine kinase (CK), aldolase, LDH, AST, and potassium. Eventually, the Na+K+ATPase pump and Ca transport takes the hit resulting in increased intracellular calcium and muscle injury. Calcium also activates intracellular enzymes including proteases inducing production of free oxygen radicals. 


Pathophysiology of Rhabdomyolysis

Potential causes of rhabdomyolysis include:


  • Alcohol (Prolonged immobilisation and direct alcohol related toxicity, Low K/Mg/PO4 also predispose)
  • Recreational Drug use (Cocaine, Amphetamines, Opoids)
  • Medications (Statins, TCAs, SSRIs, Lithium, Steroids, MAOi )
  • Myopathies(Dermatomyositis, Polymyositis)
  • Trauma (Electricity, Crush Injury)
  • Seizures
  • Prolonged Immobility (Post Falls in Elderly)
  • Infection (Bacterial and Viral)
  • Strenuous physical activity
  • Heat-related illness. 



Inherited metabolic disorders should be suspected with recurrent episodes of rhabdomyolysis



Clinical Presentation
  • Acute onset muscle aches
  • Muscle stiffness and weakness
  • Fever
  • Dark coloured urine. 
  • Nausea, vomiting and tachycardia 
  • Tenderness Muscles 

Examination may be completely normal. Therefore, look for cues in the history and work up based on that.


Diagnosis

Raised CK is a marker of muscle injury. The degree of elevation correlates with the amount of damage but it is unrelated with the morbidity. A rise in CK >5 times than normal is considered as significant. CK levels begin to rise 2 to 12 hours after the onset of injury, and peak within 24 to 72 hours.


Pattern of Myoglobin and CK rise during Rhabdomyolysis


Myoglobin elevation actually occurs before CK elevation but it rapidly cleared from the plasma. It enters urine only when the plasma concentration is significantly elevated. Because myoglobin contains heme, dipstick tests may turn positive as then test cannot differentiate among hemoglobin, myoglobin, and red blood cells. Therefore, suspect myoglobinuria when the urine dipstick test is positive for blood but no red blood cells are present on microscopic examination. 


Myoglobin levels may return to normal within 1 to 6 hours after the onset of muscle necrosis, therefore absence of an elevated serum myoglobin level or of myoglobinuria does not exclude the diagnosis. 

Due to cellular injury, serum electrolyte disturbances are seen commonly (Low Ca, High K/Uric Acid/Phosphorus). Renal Function tests reflect the extent of kidney injury. 


Management

  • Treat the underlying cause
  • Aggressive Fluid Resuscitation (Normal Saline)
  • Target Urine Output is 200-300ml/hr (catheterise to check output in critically ill)
  • Treat Hyperkalemia with usual measures
  • Avoid Nephrotoxic Medications 
  • Renal Replacement therapy
  • Consider mannitol, especially if compartment syndrome - Low grade evidence 

As usual - Bicarbonate is recommended by some but without any definite evidence base. 


The idea of urine arlkalinization stems from the fact that myoglobin precipitation is increased in acidic urine. However, in clinical studies - urine alkalinization has not been shown to impact outcomes. 

  

Compartment syndrome and peripheral nerve injury are potential mechanical complications of Rhabdomyolysis. Rarely, thromboplastin release from damaged muscle leads to consumptive coagulopathy and DIC. 



Take Home

  • Early recognition and prompt initiation of treatment is the key
  • Pick cues from the history as examinations findings can be subtle or absent
  • Watch for the complications (DIC, Compartment Syndrome)


References:
  1. Parekh R, Care DA, Tainter CR. Rhabdomyolysis: advances in diagnosis and treatment. Emergency medicine practice. 2012 Mar;14(3):1-5.
  2. Malinoski DJ, Slater MS, Mullins RJ. Crush injury and rhabdomyolysis. Critical care clinics. 2004 Jan 1;20(1):171-92.
  3. Giannoglou GD, Chatzizisis YS, Misirli G. The syndrome of rhabdomyolysis: pathophysiology and diagnosis. European journal of internal medicine. 2007 Mar 31;18(2):90-100.
  4. ThomasR:Towardsevidence-basedemergencymedicine: bestBETS from the Manchester Royal Infirmary. Emerg Med J 27: 305, 2010. 
  5. Dalakas MC: Toxic and drug-induced myopathies. J Neurol Neurosurg Psychiatry 80: 832, 2009.
  6. Clarkson PM, Eichner ER: Exertional rhabdomyolysis: does elevated blood creatine kinase foretell renal failure? Curr Sports Med Rep 5: 57, 2006. [PMID: 16529674]
  7. Vanholder R, Sever MS, Ekrem E, et al: Rhabdomyolysis. J Am Soc Nephrol 11: 1553, 2000. 

Posted by:

              
     Lakshay Chanana
     
     Speciality Doctor
     Northwick Park Hospital
     Department of Emergency Medicine
     England

     @EMDidactic