Community EM

Catatonia

Case

An 82 year-old female presents to the ED with her daughter due to altered mental status. On EMS arrival to the patient’s home, she is somnolent and unable to speak. She is activated as a Code Stroke and brought immediately to CT scan upon arrival. After returning from the CT scan, you go in to perform a comprehensive neurologic exam. The patient is lying in bed with her eyes closed, she does not arouse to voice. She does grimace with painful stimulation such as sternal rub. She groans and mumbles words but does not make coherent sentences. She does not follow commands. Her extremities do localize to painful stimulation. Despite her concerning neurologic exam, she is maintaining O2 saturations at 98% on room air and a respiratory rate of 14 with full deep breaths. While performing her neurologic exam, you lift her arm into the air and she holds it there indefinitely until you move the arm again. The radiologist calls to inform you of her normal non-contrast CT and CTA of the brain and neck. All laboratory work returns reassuring. On re-examination, she continues leave her limbs in the exact position you place them in until re-positioned. This reminds you of a condition that you learned about in medical school… catatonia!


Clinical Presentation

Catatonia is a syndrome characterized by psychomotor abnormalities and often associated with a variety of psychiatric and neurologic conditions, classically schizophrenia. The syndrome can present with a variety of psychomotor symptoms and often decreased mental state. Although it was originally thought to be associated solely with schizophrenia, it has now been found to be associated with any psychiatric condition including PTSD, bipolar disorder, depression as well as neurologic conditions such as encephalitis, stroke, malignancy, or dementia. Catatonia can be a difficult diagnosis to make due to a variety of presentations. Some of the classic features of catatonia are listed below.


In the DSM-V definition of catatonia, the patient must present with at least three of the following:

  • Stupor – overall decreased activity or decreased interaction with the environment

  • Catalepsy – muscular rigidity, i.e. a limb stays where it is positioned

  • Waxy flexibility – resistance to positioning, like a feeling of bending a candle

  • Mutism – no verbal response

  • Negativism – no response to external stimuli

  • Posturing – maintaining a specific position for prolonged periods of time

  • Mannerisms – odd movements

  • Stereotypy – repetitive movements

  • Agitation

  • Grimacing

  • Echolalia – mimicking speech

  • Echopraxia – mimicking movements


Diagnosis

The diagnosis of catatonia is based on recognition of these classic clinical findings. Appropriate medical workup to exclude organic etiology is also very important. For example, common mimics could include acute intracranial processes such as ischemic or hemorrhagic stroke, meningitis/encephalitis, electrolyte derangement, neuroleptic malignant syndrome, serotonin syndrome, delirium, and many other causes. Consideration to medical workup to exclude these causes is of utmost importance to make the diagnosis and not miss a life-threatening process. Detailed history and physical exam should be performed, including specific attention to complete neurologic exam, evaluation of reflexes, and any signs of autonomic instability. Additional testing should include broad laboratory work, brain imaging including CT or MRI, and consideration of CSF studies.

 

Treatment

Once a diagnosis of catatonia is suspected, the treatment should be initiated as soon as possible. The simplest treatment for an ED physician to perform is termed the “benzodiazepine challenge.” This can help with diagnostic uncertainty and rapidly improve symptoms in a majority of patients. Lorazepam is most often cited as the agent of choice due to its evaluation in the literature and the ease of use for ED physicians. It is estimated that about 60-80% of patients will achieve remission with benzodiazepine monotherapy. In a patient with suspect catatonia, the ED physician can give 2 mg IV lorazepam and observe the patient. Rapid improvement can be seen in their symptoms within a few minutes. After approximately 20-30 minutes, the patient may have recurrence of their catatonia symptoms and regress. Additional IV lorazepam can be given as needed. Besides IV benzodiazepines, the alternative treatment of choice is ECT. This should be started as soon as feasible, ideally within 24 to 48 hours of diagnosis. Antipsychotic drugs should be avoided in patients with catatonia, even for aggression or agitated patients.  If not properly and promptly treated catatonia can proceed to malignant catatonia which carriers an associated mortality of up to 20%.

 

Disposition

All patients with suspected diagnosis of catatonia should be admitted to the hospital for aggressive management of catatonia as well as the underlying psychiatric or medical disorder. Patients who have autonomic instability or hyperthermia should be admitted to the intensive care unit for close supportive care. Long term catatonia carriers a favorable prognosis.

 

Case Conclusion

Our patient was given a single dose of 1 mg IV lorazepam and soon after, began to speak and interact with her daughter, who had accompanied to the ED. Within one hour, she had return of mutism and cataplexy so an additional dose of IV lorazepam was given with rapid improvement of her symptoms. She was admitted to internal medicine with psychiatry consulting and was transitioned to an oral lorazepam regimen. She ultimately had good recovery and was discharged back to home with her daughter after an inpatient stay.

  

Teaching points

  • Catatonia is a purely clinical diagnosis that can be made in the ED

  • Recognize the characteristic clinical findings to keep this syndrome on your differential diagnosis of patients with mental changes

  • The treatment of catatonia should be initiated in the ED with IV lorazepam and rapid clinical improvement can help confirm your diagnosis


Faculty Reviewer: Dr. Kristina McAteer


References

  1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), American Psychiatric Association, Arlington 2013

  2. Fink, Max, and Michael A. Taylor. "The many varieties of catatonia." European archives of psychiatry and clinical neuroscience 251.1 (2001): I8-I13.

  3. HUANG, TIAO‐LAI. "Lorazepam and diazepam rapidly relieve catatonic signs in patients with schizophrenia." Psychiatry and clinical neurosciences 59.1 (2005): 52-55.

  4.  Jaimes-Albornoz, Walter, and Jordi Serra-Mestres. "Catatonia in the emergency department." Emerg Med J (2012): emermed-2011. 

  5. Sharma, Puja, et al. "Catatonia in patients with dementia admitted to a geriatric psychiatry ward." Journal of neurosciences in rural practice 8.Suppl 1 (2017): S103.

  6. Wilcox, James Allen, and Pam Reid Duffy. "The syndrome of catatonia." Behavioral Sciences 5.4 (2015): 576-588.

Cases from the Community: Springing a Leak

Case

A 58 year-old male, with history of kidney stones and appendectomy, presents to the ED with complaint of left lower quadrant abdominal pain. The patient goes on to describe waxing and waning “deep” and moderately severe pain in the abdomen with radiation to the back for two days. He notes associated nausea and one episode of dark urine but denies any fevers, nausea, vomiting, diarrhea, or any other urinary symptoms. He reports the pain is similar to prior episode of kidney stones, but feels more anterior.

Vital Signs

BP 177/93 | Pulse 87  | Temp 98.1 °F (36.7 °C)  | Resp 20  | SpO2 97%

Exam
Constitutional: Well-developed, in no apparent distress.

Cardiovascular: Normal rate and regular rhythm.  

Pulmonary/Chest: Effort normal and breath sounds normal. He has no wheezes. He has no rales.

Abdominal: Soft. Focal left local quadrant tenderness, No rebound, rigidity or guarding.  

GU: Normal testicular lie, no tenderness or erythema of the testicles. Normal cremasteric reflex. No costovertebral angle  tenderness.

Workup

Labs performed including complete blood count and basic metabolic profile are within normal limits, with a creatinine of 0.74. Urinalysis demonstrates 10 red blood cells, 1 white bell cells, and is otherwise within normal limits.

Given the patient’s significant abdominal pain, Computed tomography (CT) abdomen/pelvis with contrast is performed:

Image 1.png
Figure 1: Axial and coronal views of the CT abdomen/pelvis.

Figure 1: Axial and coronal views of the CT abdomen/pelvis.

Diagnosis

Spontaneous calyceal rupture

Radiologic impression

Mild left hydronephrosis, with moderate to severe perinephric and lower left retroperitoneal fluid concerning for recent calyceal rupture. No discrete obstructing calculus currently visualized. Of note, there is a 1.1 cm calculus in the left renal pelvis. In addition, given, extensive fluid, superimposed infection cannot be excluded.

Discussion

The above case is a classic example of a not-too-common urologic finding in the ED: spontaneous calyceal rupture. This finding is thought to occur as a result of a sudden increase in pressure in the collecting system. Most commonly, this sudden increase pressure is due to an obstructing kidney stone (typically in the distal ureter), however, it has also been described in the setting of other pathologies that obstruct the urinary system, including cancer, prostatic hypertrophy, pregnancy, and abdominal aortic aneurysm, as well as iatrogenic causes. The collecting system, typically a low-pressure system, is poorly equipped to handle the sudden increase in pressure, and ruptures in the most susceptible part of the system — the calyx. More specifically, it is the fornix, the lateral aspect of the minor calyx, that is the most common culprit (Figure 1).

Figure 2: Anatomy of the kidney.

Figure 2: Anatomy of the kidney.

Most cases of calyceal rupture present with flank pain, nausea, and vomiting, although more severe symptoms, such as severe abdominal pain and systemic findings, can occur. Rupture results in extravasation of urine that can collect around kidney or even in the retroperitoneum. The feared complication of this process is infection of the urine collection, leading to perinephric abscess formation and sepsis. The diagnosis is made either via ultrasound or CT.

Management first involves relieving the cause of obstruction. In the ED, if the obstruction is secondary to prostatic hypertrophy a foley should be placed. The patient should receive hydration and analgesia. Urology should be consulted to understand which patients will need intervention such as stenting or lithotripsy. At this time there is no standard as to the appropriateness of antibiotic therapy. Of course, if a patient shows evidence of infection, antibiotics (and source control) are indicated. However, if a patient demonstrates no systemic signs of infection and has a negative urinalysis it is reasonable to consider deferring antibiotics at the index visit. This decision, as well as whether to admit or discharge the patient should be made in conjunction with our urology colleagues.

Case conclusion

The patient was managed conservatively with fluids and analgesia. Antibiotics were deferred in consultation with Urology. The patient was discharged to close urologic follow-up. At four month chart review the patient had suffered no further complications and no long term sequelae from his calyceal rupture.  

 Faculty Reviewer: Dr. Kristy McAteer


References

  1. Al-Mujalhem AG, Aziz MS, Sultan MF, Al-Maghraby AM, Al-Shazly MA. Spontaneous forniceal rupture: Can it be treated conservatively? Urol Ann 2017:9(1);41-44 

  2. Doehn C, et al. Outcome analysis of fornix ruptures in 162 consecutive patients. J Endourol 2010;24(11):1869-73.

  3. Morgan TN, Bandari J, Shahait M, Averch T. Renal forniceal rupture: Is conservative management safe? Urology 2017;109:51-54.

  4. Tanwar S, Joshi A. A blow-out. Am J of Med 2011;124(1):37-39.

  5. https://opentextbc.ca/anatomyandphysiology/chapter/25-3-gross-anatomy-of-the-kidney/

Fibrinolytic Therapy for STEMI

Case

You are on a swing shift at a remote, island-based community hospital when a 58 year-old male presents with sudden onset chest pain. The pain started at rest, radiates to his jaw, and is associated with diaphoresis and nausea. He has a history of coronary artery disease (CAD), and during his last cardiac catheterization in 2008, a stent was placed in his proximal left anterior descending coronary artery. His past medical history is also significant for diabetes, chronic obstructive pulmonary disease, hyperlipidemia, and hypertension.  He is an active smoker.

On exam, he is not only diaphoretic and clenching his chest, but also describes the pain as “an elephant sitting on my chest.” Initial vital signs are P 110, BP 175/100, RR 20, PO2 98% on RA, T 98.9 F. You give him aspirin 324 mg and nitroglycerin sublingual 0.4 mg, and his chest pain improves from a 10/10 to 8/10. His initial electrocardiogram (EKG) is below.

Figure 1: The patient’s presenting EKG.

Figure 1: The patient’s presenting EKG.

DIAGNOSIS

ST elevation myocardial infarction (STEMI)

Management Options

You call the critical care transport ambulance, as well as the nearest cardiac catheterization team to alert them of your patient.   Unfortunately, it is a stormy evening in the middle of winter and all bridges off the island are closed; helicopters are grounded due to the storm.  There are no transfer options available to your patient at this time. What else can you do?

Indications for Fibrinolytic Therapy

According to the American Heart Association, there are several considerations when it comes to fibrinolytic therapy in myocardial infarction:

Class I recommendations:

  1. STEMI

  2. Symptom onset in the last 12 hours

  3. Percutaneous Cardiac Intervention (PCI) cannot be performed within 120 minutes of arrival to the Emergency Department

  4. Absence of any contraindications (see below)

Class II recommendations:

  1. Evidence of ongoing ischemia 12-24 hours after symptom onset

  2. Large area of myocardium affected

  3. Hemodynamic instability

Absolute contraindications:

  1. Any prior intracranial hemorrhage

  2. Known structural cerebral vascular lesion

  3. Ischemic stroke <3 months

  4. Suspected aortic dissection

  5. Known intracranial malignancy

  6. Active bleeding or bleeding diathesis

  7. Significant closed head trauma <3 months

  8. Intracranial/intraspinal surgery <2 months

  9. Severe uncontrolled HTN (>175/110)

  10. Oral anticoagulants

Relative contraindications:

  1. Significant HTN on arrival (pressure > 180 mmHg)

  2. Ischemic stroke >3 months

  3. Dementia

  4. Other intracranial pathology

  5. Traumatic CPR >10 min

  6. Major surgery <3 weeks

  7. Internal bleeding <3 weeks

  8. Non-compressible vascular punctures

  9. Pregnancy

  10. Active peptic ulcer disease

PCI versus Systemic Fibrinolytic Therapy

If you are able to transfer the patient to a hospital with PCI capability within 1 hour of presentation or they have contraindications to fibrinolytic therapy, it is recommended that you transfer the patient as soon as possible. Otherwise, the goal is fibrinolytic infusion within 30 minutes of arrival to the ER. In either case, concurrently initiate maximal medical management including full-dose aspirin, Plavix or Brilinta, and anticoagulation (unfractionated heparin or lovenox). Tenecteplase is generally the preferred fibrin-specific agent, given its ease of use and lower rates of non-cerebral bleeding compared to other agents.

Reassess After Fibrinolysis

If your patient has resolution of chest pain and >70% reduction of ST elevation, or ST elevation resolves within 60-90 minutes, you have likely restored flow. If you see <50% decrease in STE and no reperfusion arrhythmias (see below) at 2 hours after fibrinolytic dosing, you have partially improved flow but not completely restored it.

Criteria for Transfer after fibrinolytic therapy

  1. Immediate transfer: acute heart failure or cardiogenic shock

  2. Urgent transfer: failed reperfusion or reocclusion

  3. 3-24 hours: hemodynamically stable, successful reperfusion

Reperfusion Arrhythmias 

You plan for ICU admission because you are unable to transfer the patient to a PCI center when the nurse hands you the following EKG:

Figure 2: Accelerated idioventricular rhythm.

Figure 2: Accelerated idioventricular rhythm.

This is an example of accelerated idioventricular rhythm. This is a normal sign of reperfusion after STEMI and does not require treatment.   In fact, such a rhythm is generally viewed as a positive response to fibrinolytic therapy as indicates reperfusion. 

Criteria:

  1. Regular rhythm

  2. Rate 50-110bpm (slower is ventricular escape, faster is VT)

  3. Three or more ventricular complexes

  4. Fusion (F) and capture (C) beats (see below)

Figure 3: Fusion and capture beats after successful reperfusion.

Figure 3: Fusion and capture beats after successful reperfusion.

General goals of care after fibrinolytic therapy should be to transfer for diagnostic angiography and percutaneous coronary evaluation which is promptly accomplished for your patient the following day after the storm resolves.


Faculty reviewer: Dr. Kristina McAteer


References

  1. O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013; 127:529.

  2. O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013; 127:e362.

  3. White HD. Thrombolytic therapy in the elderly. Lancet 2000; 356:2028.

  4. Armstrong PW, Gershlick AH, Goldstein P, et al. Fibrinolysis or primary PCI in ST-segment elevation myocardial infarction. N Engl J Med 2013; 368:1379.

  5. Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI). Lancet 1986; 1:397.

  6. Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Lancet 1988; 2:349.
    Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomised trials of more than 1000 patients. Fibrinolytic Therapy Trialists' (FTT) Collaborative Group. Lancet 1994; 343:311.

  7. Labinaz M, Sketch MH Jr, Ellis SG, et al. Outcome of acute ST-segment elevation myocardial infarction in patients with prior coronary artery bypass surgery receiving thrombolytic therapy. Am Heart J 2001; 141:469.

  8. Peterson LR, Chandra NC, French WJ, et al. Reperfusion therapy in patients with acute myocardial infarction and prior coronary artery bypass graft surgery (National Registry of Myocardial Infarction-2). Am J Cardiol 1999; 84:1287.

  9. Karnash SL, Granger CB, White HD, et al. Treating menstruating women with thrombolytic therapy: insights from the global utilization of streptokinase and tissue plasminogen activator for occluded coronary arteries (GUSTO-I) trial. J Am Coll Cardiol 1995; 26:1651.

  10. Woodfield SL, Lundergan CF, Reiner JS, et al. Angiographic findings and outcome in diabetic patients treated with thrombolytic therapy for acute myocardial infarction: the GUSTO-I experience. J Am Coll Cardiol 1996; 28:1661.

  11. Mak KH, Moliterno DJ, Granger CB, et al. Influence of diabetes mellitus on clinical outcome in the thrombolytic era of acute myocardial infarction. GUSTO-I Investigators. Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries. J Am Coll Cardiol 1997; 30:171.