Monday, March 28, 2016

Uterine Rupture - An obstetric catastrophe

Uterine rupture is defined as a non-surgical disruption or tear of the myometrium and serosa of the uterus with or without expulsion of the fetus. It is a life threatening condition for both the mother and the fetus. The overall incidence of uterine rupture is low but in India and other developing nations, it is 10 fold higher.

  • Scarred Uterus Rupture: Previous caesarean scar or myomectomy
  • Unscarred Uterus Rupture: Obstructed labour, Trauma, Grand-multiparty, Uterine anomaly or injudicious use of oxytocin or prostaglandins

Clinical Features
  • Severe haemorrhage, Tachycardia, Hypotension (Shock)
  • Palpable fetal parts with loss of fetal station
  • Recession of presenting fetal parts
  • Prolonged, Persistent, Profound fetal bradycardia
  • Loss of uterine contractility
  • Hematuria
  • Appearance of placenta at vulva 
  • Prolapsed loops of gut into vagina 

Typically seen in patient with history of CS but also possible in Primigravida

USG: Fetus in peritoneal cavity, Free fluid seen

Differential Diagnosis
  • Abruptio Placentae (Similar presentation)
  • Hepatic Rupture in severe pre eclampsia (Look for other signs of pre-eclampsia)
  • Chorioamnionitis (Look for fever, PROM, Tender uterus)

ABC (Wide bore cannulas, fluids, O2, Blood Products)
Stop oxytocin if in progress
Type and Cross Match
Mobilising resources quickly is the key (OBGYN, Anaesthesia, Neonatology)
Immediate laparotomy is indicated 
  • Vertical incision gives better access
  • Fetus lies partially or completely in the abdominal cavity
  • Rent repair or hysterectomy are the surgical options depending on the degree of rupture and damage
Several studies have shown that delivery of the fetus within 10-37 minutes of uterine rupture is necessary to prevent serious fetal morbidity and mortality.

Take Home
  • When dealing with trauma in pregnancy, think Placental Abruption and Uterine Rupture (Both can co-exist)
  • Establishing diagnosis early and mobilising the resources quickly and effectively results in favourable outcomes for the mother and fetus

For further reading:
  1. Qudsia, Q. A. Z. I., et al. "Woman health; uterus rupture, its complications and management in teaching hospital bannu, pakistan." Maedica 7.1 (2012): 49.
  2. Blanchette H, Blanchette M, McCabe J, Vincent S. Is vaginal birth after cesarean safe? Experience at a community hospital. Am J Obstet Gynecol. 2001 Jun. 184(7):1478-84; discussion 1484-7.
  3. Leung AS, Leung EK, Paul RH. Uterine rupture after previous cesarean delivery: maternal and fetal consequences. Am J Obstet Gynecol. 1993 Oct. 169(4):945-50. 
  4. Yap OW, Kim ES, Laros RK Jr. Maternal and neonatal outcomes after uterine rupture in labor. Am J Obstet Gynecol. 2001 Jun. 184(7):1576-81
  5. Essentials of Obstetrics - Lakshmi Seshadri and Gita Arjun
  6. Batra, Kanika, et al. "Determinants of rupture of the unscarred uterus and the related feto-maternal outcome: current scenario in a low-income country." Tropical doctor (2015): 0049475515598464.
  7. A Massinde, E Ndaboine, A Kihunrwa. An unusual case of placenta abruption complicated with ruptured uterus: case report. The Internet Journal of Gynecology and Obstetrics. 2009 Volume 13 Number 1.


   Kritika Atrey 
   Aarupadai Veedu Medical College
   Twitter: @atrey_kritika

   Edited by Lakshay Chanana @EMDidactic

Monday, March 21, 2016

Foreign Body Aspiration masquerading as Pneumonia


Two and a half year old boy presented to the ER with a seizure. Mother gave h/o cough cold, fever for the past one week and the child also had history of a choking spell one week back. Background h/o reactive airway disease (RAD) was positive.

O/E: Dehydrated , Comatose, Gasping

HR 60bpm, RR 50bpm , SpO2 60% RA, Temp 103F and bilateral silent chest .Vitals improved with BMV and he was treated on the lines of infective exacerbation of reactive airway disease. 

CXR on arrival

Eventually he was intubated following which SpO2 improved to 94%. CXR was suggestive of left consolidation /collapse. He was shifted to the ICU where due to a lack of response to treatment, he underwent bronchoscopy that revealed a peanut that caused collapse of the left lung and secondary infective exacerbation of RAD.

CXR after 2 days


Foreign Body Aspiration (FBA) occurs commonly in children and it is frequently encountered by paediatric EM practitioners. It is more common in boys and frequently seen in kids less than 3 years of age. With classic acute and dramatic presentations, FBA is usually frequently diagnosed promptly but the diagnoses can get delayed with subtle of atypical presentations if a high index of suspicion is not maintained. 

Classic history comes as choking, coughing and cyanosis. Examination may reveal respiratory distress, asymmetrical chest expansion, localised wheeze or decreased breath sounds. If the size of the FB is small in relation to the airway, it can lead to partial airway obstruction and presentation may be delayed for days or weeks ultimately presenting as pneumonia. Majority of the FB aspirated are organic materials typically peanuts which can gradually absorb water and swell up over a period of time leading to complete obstruction. Inorganic FB like batteries, coins, toys are rare (unfortunately, the rare ones are easily seen on a CXR). 

Even with a FBA, CXR can be completely normal or it may show air trapping, infiltrates, consolidation. A later CXR may help in differentiating between airway and oesophageal FB. CT scans and bronchoscopy can further accurately localise the FB and aid removal . Whenever there is a high suspicion (based on history or poor response to treatment), further work up must be done. Rigid Bronchoscopy is used for the definitive management with occasional use of flexible bronchoscopes to reach sub segmental FBs

Take Home:
Aspirated foreign body is an important differential diagnosis for Asthma/Reactive Airway Disease and should also be considered in the child who has an exacerbation that does not respond to standard treatment. 

Further Reading
1. Rizk H, Rassi S. Foreign body inhalation in the pediatric population: lessons learned from 106 cases. Eur Ann Otorhinolaryngol Head Neck Dis 2011;128(4):169-174.
2. Asif M, Shah SA, Khan F, Ghani R. Analysis of tracheobronchial foreign bodies with respect to sex, age, type and presentation. J Ayub Med Coll Abbottabad 2007;19(1):13-15.
3. Saki N, Nikakhlagh S, Rahim F, Abshirini H. Foreign body aspirations in infancy: a 20-year experience. Int J Med Sci 2009 14;6(6):322- 328.
4. Fraga Ade M, Reis MC, Zambon MP, Toro IC, Ribeiro JD, Baracat EC. Foreign body aspiration in children: clinical aspects, radio- logical aspects and bronchoscopic treatment. J Bras Pneumol 2008;34(2):74-82.
5. Orji FT, Akpeh JO. Tracheobronchial foreign body aspiration in children: how reliable are clinical and radiological signs in the diagnosis? Clin Otolaryngol 2010;35(6):479-485.
6. Jung SY, Pae SY, Chung SM, Kim HS. Three-dimensional CT with vir- tual bronchoscopy: a useful modality for bronchial foreign bodies in pediatric patients. Eur Arch Otorhinolaryngol 2011;16. (Epub ahead of print)
7. Passàli D, Lauriello M, Bellussi L, Passali GC, Passali FM, Gregori D. Foreign body inhalation in children: an update. Acta Otorhinolaryn- gol Ital 2010;30(1):27-32.
8. Wu CT, Wang CJ. Alternate lung collapse in a 9-year-old boy with peanut aspiration. Pediatr Radiol 2006;36(12):1327. 
9. Zaupa, Paola, et al. "Management strategies in foreign-body aspiration." The Indian Journal of Pediatrics 76.2 (2009): 157-161.
10. Cohen, Shlomo, et al. "Suspected foreign body inhalation in children: what are the indications for bronchoscopy?." The Journal of pediatrics 155.2 (2009): 276-280.

Case contributed by Dr. Azharullah Khan, MRCEM (@Khan123Azhar)

Monday, March 14, 2016

The shunned nursing note

Quality documentation is a integral part of our job. The care that we provide is always judged by the kind of documentation that we do. 

If a thing is not documented, it is not done. 

At the same time, there is something very unusual here, a big disconnect between the physicians and the nurses. I have always witnessed nurses checking out and reading a physician's note but a physician reading a nursing chart is a rare sight. Most of you would agree that physicians do not pay much attention to the nursing notes unless they are in the soup. And if you ask me why do physicians do this, I would say that this can be a multitude of reasons for doing that like a physician's ego, lack of trust, lack of a rapport or they just don't care about what nurses document. 

Everything goes smooth until and unless there is a mishap and a lawsuit. And in the court of law the documentation done by the physicians as well as the nurses is frequently scrutinised to review the case and understand the timelines. Things can really go out of the track  because of a mismatch between our notes. So, the importance of nursing notes cannot be underestimated. 

As compared to a doctor's documentation, nursing documentation is much more comprehensive in terms of the vital signs monitoring, communication and ongoing patient care. In my opinion, a nursing note is far more detailed, legible and honest. Next time, have a glance through their note and you will be surprised to find that how thorough they can get. You will find every minute aspect of patient care documented like assessment, what the patient exactly said, monitoring, counselling, teaching, medications, verbal and written orders, compliance, evaluation , plan and communication about all this with the physician. You might also find your name documented in their note! 

So, don't you think we should pay a bit more attention towards all their hard work? If not for all the patients, at least for those who are getting discharged from the ED  and for the ones who are critically ill.

When evaluating a patient in the ED, we need to remember that the documentation actually starts from the field followed by triage notes, nursing assessment and then the physician notes. Our responsibility then is to do our own history and physical rather than duplicating the same notes again. It is also crucial to be aware of the timelines and make sure that there are no discrepancies between the physician's and the nursing note. If there is a discrepancy, then mention that in your chart with reference to the nursing note to make sure the message is conveyed clearly. 

A typical nursing note: (it can get much more detailed)

14/03/2015  0900hrs Patient received on Bed No. 4. He is alert and oriented to time, place and person. Complaining of headache. No H/O Allergies. VS: PR 98/min  BP 110/74  RR 14/min SpO2 99% RA, Afebrile. Inj.  Acetaminophen 1gm IV given over 30 minutes through left ante cubital vein. Monitored continuously for medication effects and adverse effects. No other concerns verbalised at this point. Informed to the resident physician (Dr. XYZ) on shift. 

14/03/2015 1130hrs Patient now complains of severe pulsating type of headache and nausea. Says "This is the worst possible headache he has experienced so far". Looks distressed. VS: PR 108/min BP 150/88 RR 17/min SpO2 98% RA Temp -100F. Informed to the on duty physician (Dr. XYZ) STAT. Inj. Ondansetron 8mg IV and Inj. Fentanyl 50mcg IV administered. Patient seen by the physician and is scheduled to undergo a Non-Contrast Head CT scan. To be shifted to CT room on call.

The key point that I want to highlight here is that doctors and nurses need to start communicating well with each other. For physicians, it is good to have a sense and understanding about nursing documentation. 

Take Home:
  • As physicians, make a habit of going through the notes of other healthcare providers (nurses/ paramedics) prior to discharging a patient and be on the same page with them.
  • Good communication will improve patient care and prevent litigation.
  • Documentation is not just for our self defence but also to foster patient care. 

For further reading:

Monday, March 7, 2016

Status Epilepticus - Rapid Review

Status Epilepticus (SE) is the second-most frequent life-threatening neurological emergency after stroke that bears considerable risks of morbidity and mortality. SE requires emergent, targeted treatment to reduce patient morbidity and mortality but the treatment strategies vary substantially from one institution to another due to the lack of data to support one treatment over another. Rapid control of seizures is fundamental to the emergency treatment of SE. Adverse effects may include systemic problems arising from seizures (e.g., impaired ventilation, pulmonary aspiration, and metabolic aberrations) or due to direct neuronal cellular injury from excitotoxicity. 

Definition and Classification
  • SE is defined as 5 min or more of continuous clinical and/or electrographic seizure activity or recurrent seizure activity without recovery between seizures
  • SE is further classified as either convulsive SE (convulsions that are associated with rhythmic jerking of the extremities) or non-convulsive SE (seizure activity seen on EEG without the clinical findings associated with convulsive SE)
  • Refractory SE (RSE) should be defined as SE that does not respond to the standard treatment regimens, such as an initial benzodiazepine followed by another AED. Although some experts consider failure of the first drug i.e. BZD to terminate seizure as RSE.

Rationale for changing the traditional 30 minutes definition to 5 minutes 
Animal data suggests that permanent neuronal injury may occur before the traditional definition of 30 min of continuous seizure activity have passed. Evidence also demonstrates that seizures that do not cease in 5-10 minutes are less likely to terminate without intervention (Pharmacoresistance).


In short - excess excitation and reduced inhibition. However, the failure of inhibitory processes is increasingly thought to be the major mechanism leading to SE.

Excitatory neurotransmitters: Glutamate, NMDA
Inhibitory neurotransmitters: GABA

Most seizures terminate spontaneously within several minutes but with continuing seizures, inhibitory GABA receptors are internalized in clathrin coated vesicles and at the same time, excitatory N-methyl-d-aspartate (NMDA) receptors may be mobilized to the membrane. This receptor trafficking results in a decreased inhibitory control and increased excitation that may lead to continuing status epileptics. The internalization of GABA receptors may explain the clinical finding that benzodiazepines are less effective as seizure durations increase.

Possible Etilogy
  • AED Non-Compliance
  • Stroke 
  • Hypoxic injury, Traumatic Brain Injury
  • Drugs and Toxins (eg, cocaine, theophylline, INH)
  • Withdrawal (Opioid, BZD, Barbiturates, Alcohol)
  • Electrolyte abnormalities 
  • Renal Failure, Liver Failure
  • Neoplasms
  • CNS infections (eg, meningitis, brain abscess, encephalitis)
  • Autoimmune Encephalitis


All patients need a 
  • Fingerstick glucose
  • Vital signs monitoring
  • Head computed tomography (CT) scan is required for most
  • Order laboratory test: blood glucose, complete blood count, basic metabolic panel, calcium (total and ionized), magnesium, AED levels. 
  • Continuous electroencephalograph (EEG) monitoring

Consider these based on clinical presentation
  • Brain magnetic resonance imaging (MRI)
  • Lumbar puncture (LP)
  • Comprehensive toxicology panel including toxins that frequently cause seizures (i.e. isoniazid, tricyclic antidepressants, theophylline, cocaine, sympathomimetics, alcohol, organophosphates, and cyclosporine)
  • Other laboratory tests: liver function tests, arterial blood gas, AED levels, toxicology screen (urine and blood), and inborn errors of metabolism.

The treatment of convulsive SE should occur rapidly and continue sequentially until clinical seizures are halted. The goal of treatment is to stop the seizures (both clinical and electrographic) as soon as possible. The initial treatment strategy includes simultaneous assessment and management of airway, breathing, and circulation (obtain IV access, administer O2, and securing the airway as needed), seizure abortive drug treatment, screening for the underlying cause of SE, and immediate treatment of life-threatening causes of SE (e.g., meningitis).

Benzodiazepines are the drugs of choiceLorazepam is the drug of choice for IV administration and Midazolam is the drug of choice for IM administration. Early intubation is advisable if continuous intravenous AEDs are necessary. 

Options for RSI meds include Propofol and Ketamine and this is a scenario where you might consider skipping the paralytics. If you are using them, beware of succinyl choline induced hyperkalemia in prolonged seizures or a chronic neurological illness. If you are using Rocuronium, get the continuous EEG to pick convulsions in a paralysed patient. 
The diagnostic labs are selected depending on the patient’s history and physical examination. Not every diagnostic study is required in every patient. For instance, a lumbar puncture is needed if there is any suspicion of a central nervous system (CNS) infection, but may not be required if patients gives a history of AED non-compliance.

Dosing and Considerations when using second and third line agents 

Dosing of continuous infusion AEDs for RSE should be titrated to cessation of electrographic seizures or burst suppression.

Propofol comes with issues like severe hypotension and propofol related infusion syndrome. Midazolam appears to be safer and less hypotensive. Be prepared to start a vasopressor drip to maintain blood pressure or switch to ketamine.

Alternative therapies: Reserve these therapies for patients in RSE
  • Ketamine (3 mg/kg IV followed by an infusion of at least 1 mg/kg/hr up to 10 mg/kg/hr.)
  • Hypothermia
  • Inhales Anesthetics (Isoflurane)
  • Ketogenic Diet
  • Steroids, ACTH
  • Immunomodulation (IVIG or Plasma Exchange)
  • Electroconvulsive therapy
  • Vagus Nerve Stimulation
  • Repetitive Transcranial Magnetic Stimulation
  • Surgical Management

     Medications are more likely to terminate seizures when given closer to the seizure onset and they decrease in effectiveness as seizure duration increases, most likely related to changes in the neuronal gamma aminobutyric acid (GABA) receptor subunit composition as a function of time. 

Rationale for using Ketamine 
There is growing evidence that increasing refractoriness to treatment is partly the result of progressive impairment of GABA mediated inhibition as a result of internalization of GABA receptors under conditions of sustained excitability. Due to this internalisation  , GABAergic drugs dare less likely to work for sustained SE. There is also evidence for increased numbers of N-methyl-D-aspartic acid (NMDA) receptors at the synaptic membrane that results in increased sensitivity to excitatory neurotransmitters. The rationale behind using Ketamine is an attempt to antagonise the excitatory NMDA system as GABAergic system is impaired. 

Take Home

  • Seizure onset to drug delivery time is more important then debating which BZD works better. Be aggressive while treating SE because pharmacoresistance develops over minutes.
  • Never forget that NCSE can present as coma and maintain a low threshold for obtaining a bedside EEG. 
  • Ketamine is definitely an option for refractory status epilepticus. 

Further Reading:

  1. Shinnar S, Berg AT, Moshe SL, Shinnar R. How long do new-onset seizures in children last? Ann Neurol 2001;49:659-64. 
  2. Gaspard N, Foreman B, Judd LM, et al. Intravenous ketamine for the treatment of refractory status epilepticus: a retrospective multi-center study. Epilepsia. 2013;54(8):1498-1503. doi:10.1111/epi.12247.
  3. Treatment of Refractory Status Epilepticus: Literature Review and a Proposed Protocol Nicholas S. Abend, MD and Dennis J. Dlugos
  4. Glauser, Tracy, et al. "Evidence-Based Guideline: Treatment of Convulsive Status Epilepticus in Children and Adults: Report of the Guideline Committee of the American Epilepsy Society." Epilepsy Currents 16.1 (2016): 48-61.
  5. Rossetti, Andrea O., and Thomas P. Bleck. "What's new in status epilepticus?." Intensive care medicine 40.9 (2014): 1359.
  7. Emergency Medicine Practice - Evidence Based Medicine - Clinical Decision Making In Seizures And Status Epilepticus 
  8. Lowenstein, Daniel H., and Brian K. Alldredge. "Status epilepticus." New England Journal of Medicine 338.14 (1998): 970-976.
  10. Brophy, Gretchen M., et al. "Guidelines for the evaluation and management of status epilepticus." Neurocritical care 17.1 (2012): 3-23.
Other FOAMed thoughts on Status Epilepticus: