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Case Based for January

Teaching Case: An Escalating Agitation Syndrome with Misleading Clues An 82-year-old woman with a history of chronic pain due to metastatic diffuse large B-cell lymphoma s/p radical neck and mouth dissection and G-tube placement presented to the ED with severe oral pain, nausea, worsening anxiety, and a profound sensation of “feeling toxic.” She lived alone and managed her medications independently. She reported taking multiple doses of hydrocodone/acetaminophen and diazepam over the preceding 24 hours. She was also maintained on a PRN Valium, hydrocodone and 125 mcg/hr fentanyl patch Q3 days, but instead of applying a new patch that morning, she had removed the old patch and moved it to a new location—a practice she used because she believed relocation to a location with more body fat was equivalent to replacement. She was a very low-body-weight patient, approximately 82 lbs, which heightened her sensitivity to rapid changes in opioid exposure. On arrival, her blood pressure was 179/67, with otherwise stable vitals. She remained alert and oriented but was increasingly restless and unable to remain still. Her laboratory studies—including CBC, CMP, magnesium, phosphorus, EKG CK, troponin, and TSH—were all within normal limits, and urinalysis was unremarkable. Her urine drug screen was negative for opiates and benzodiazepines, despite her reported intake of Valium and Hydrocodone. This tox panel did not test for fentanyl. Based on her symptoms and the interpretation that she may not have adequately taken her home medications, the initial working diagnosis was acute anxiety with poorly controlled pain. At 01:26 she received lorazepam 1 mg IV and morphine 2 mg IV. Shortly thereafter, she experienced a marked and abrupt deterioration: she became intensely agitated, thrashing in bed, gripping the rails, unable to sit still, and repeatedly describing the sensation of “jumping out of my skin.” Because this escalation occurred immediately…

Case Based for November & December

Catatonia A 60 year old female with history of bipolar disorder with aggressive behavior, hypertension, and chronic kidney disease, was brought in by ambulance after her husband found her unresponsive on the floor. He reports that she was diagnosed with COVID two weeks ago. She had not had anything to eat or drink for two days. Her vital signs were: T 98.9, P 72, R 16, BP 148/88, SpO2 96% on RA. She was responsive to pain in the ED and would occasionally follow commands but was never alert or able to answer questions. WBC 18.7, Na 177, glu 145, BUN 135, crt 3.71, venous pH 7.36, lactic 1.8. CT head showed no acute findings. There were no beds available at larger facilities for transfer. She was started on D10 ¼ NS @ 160ml/hr. Her mental status waxed and waned but never returned to baseline. The following day she was finally transferred to Sacred Heart, where she remains weeks later. Her sodium and renal function were corrected. She was diagnosed with psychosis with catatonia and is now on a court-ordered hold for ECT on the psych service. Discussion: Catatonia is a behavioral syndrome marked by inability to move normally due to underlying psych or general medical disorder. The signs are heterogeneous but can include immobility, mutism, decreased alertness and responsiveness, negativism (resistance to attempts to move or to instructions), waxy flexibility, posturing, excessive purposeless motor activity, staring, robotic voice, and echolalia (senseless repetition of other person’s utterances) or echopraxia (senseless repetition of other person’s movements). These patients have frequent dehydration/malnutrition, DVT/Pes, contractures, pressure ulcers, and excitement/impulsivity, which all need to be managed. Antipsychotics and dopamine blocking agents should be avoided, as they can cause neuroleptic malignant syndrome. Treatment with benzodiazepines is the mainstay, usually lorazepam 1-2mg IV TID. If there…

Case Based Learning for October 2025

Ketamine-induced Laryngospasm A 60 yo male presented for an angulated colles fracture. He was given IV dilaudid on arrival. A hematoma block was attempted, but the needle would not advance into the fracture site. Therefore, I decided to give a sub-anesthetic dose of ketamine to reduce pain during reduction. As soon as the ketamine was in, the patient’s upper body became stiff. He had a blank stare on his face and his chest stopped moving; I immediately reduced the fracture thinking the pain would initiate breathing. It did not. I let go of his arm and assisted the RN in bagging the patient. I made sure there was an excellent seal with the mask, and that the upper airway was open by performing head tilt, jaw thrust, and placing an oral airway. The pt could not be bagged; the epigastric area moved but the chest did not move with bagging. I realized that laryngospasm was preventing ventilation. O2 saturation dropped to the 77%. I ordered Ativan and the glidescope to the bedside. Then the larynx suddenly opened long enough to deliver two breaths to the lungs and the SaO2 improved. The larynx closed again for 30 seconds before reopening for a few seconds. This occurred a few times before the larynx opened and stayed open, at which time the patient breathed spontaneously and I augmented his breathing with the bag for a minute. The terrifying whole episode lasted about 6 minutes. I then placed a splint and the patient regained consciousness with complete recovery. For a few minutes, I felt like I could not continue working after the stress of this event. I went from being terrified to apprehensively hopeful that he would not be injured, to overwhelmingly grateful he was ok, all in the span of 10 minutes. I…

Case Based Learning for September 2025

A 68-year-old female presented to the ED with chest pain and shortness of breath. Her medical history was significant for hypertension, diabetes, and ESRD on dialysis for one year. She has been compliant with dialysis. Workup in the ED was significant for a junctional bradycardia in the 30s and a systolic blood pressure in the 60s. Lab work was significant for a glucose of 194, a potassium of 5.8, and a creatinine of 8.04 with a calculated GFR of 5. She was given 1mg atropine, which was ineffective. She was then started on an epinephrine infusion with minimal response. Transcutaneous pacing was initiated, and she was given pain control and sedation as her blood pressure tolerated. A tertiary care center was contacted and after an extended wait she was transferred. At the receiving hospital she was taken to the cath lab. No significant disease was noted, and a temporary venous pacemaker was placed. As her hyperkalemia was corrected and her Carvedilol wore off the pacemaker was discontinued. She was discharged home in good condition two days later. BRASH syndrome is an acronym for Bradycardia, Renal Failure, AV blockade, Shock, and Hyperkalemia. BRASH syndrome is a synergistic process created by a combination of hyperkalemia and medications blocking the atrioventricular (AV) node. The most common precipitants are hypovolemia and medications promoting hyperkalemia or renal injury. Often referred to as a vicious cycle, standard ACLS treatments may prove ineffective, as in this case. Bradycardia reduces the cardiac output; impairs renal perfusion; precipitates renal dysfunction; and exacerbates hyperkalemia. Left unchecked, the vicious cycle of hyperkalemia, bradycardia, renal dysfunction, and worsening hyperkalemia may progress to multiorgan failure with shock, bradycardia, and renal failure. The most common error in managing BRASH syndrome is fixating on a single component of the syndrome (e.g., hyperkalemia) and focusing solely…

Helping our hospitals survive: It Starts with Documentation

Many of you have asked “how can I help our rural communities maintain the access to local emergency care.” As Providers serving critical access hospitals, one of the easiest ways we can help is to properly document the care we are providing patients. Appropriately documenting helps to ensure that our time and efforts are appropriately reimbursed. As clinicians, we strive to provide appropriate evidence-based care to our patients, however we often fall short on our documentation of that care. One of the areas that most often falls short, is critical care documentation. I would like to share with you a document that one of our Washington critical access facilities disseminated to our provider team. It’s an extremely helpful guide and lists many of the common conditions that may qualify for critical care time as well discusses key items that we must document. Please reflect on each of your cases to see if critical care time could have been added. CMS Defination of Critical Care-2025august Paula Silha, MD Chief Medical Officer, ERx Clinical Partners

Case Based Learning for August 2025

46-year-old male arrived to the ED in January via EMS who reported the patient had abdominal pain and shortness of breath and was initially anxious but then fell asleep en route.  On arrival, the patient was calm and kept his eyes closed without speaking much.  He mumbled that he was having trouble breathing recently and gave vague history of recent chest pain, abdominal pain, and coughing.  The patient fell asleep during history taking but was arousable to voice.  He had been seen the day before in our ED complaining of shortness of breath.   That chart revealed he had a history of methamphetamine abuse, cardiomyopathy, LV mural thrombus on Eliquis, and PTSD.  The day before, a full cardiac workup was unremarkable and he was discharged. The patient appeared withdrawn and somnolent, not speaking much.  I considered whether he was coming off of a meth binge, and experiencing the hypersomnia and encephalopathy sometimes seen with a meth crash.  It was noted that his hands and feet were cold and cyanotic, but the medics stated that the house was very cold and perhaps cold exposure was causing vasoconstriction.  Initial blood pressure was 100/70, heart rate of 76, SaO2 97%.  Initial EKG is shown below. The workup was ordered and the patient was rechecked and condition was not improving.  Pulse ox was not showing good waveform.  The medical student called me when the patient became agitated and profusely diaphoretic.  Subsequently, the patient said “I’m going to die!”, laid back, and lost consciousness.  He continued breathing and had a very weak femoral pulse.  While trying to decide whether to begin CPR, I noted a flurry of dysrhythmias on the monitor.  There were several beats of bradycardia followed by a few multifocal PVCs followed by a very wide-complex tachycardia with giant T waves with a…

Case Based Learning for July 2025

An Unusual Cause of Urticaria ER Presentation:  A 45 y/o female arrived by EMS because she was awoken while sleeping with abdominal pain, n/v, scattered hives and dyspnea. She felt lightheaded when ambulating but there was no syncope. Pertinent negatives:  no fever, cough, chest pain, throat pain or swelling in throat. Denied possible allergen exposure. Past medical history: noncontributory. Medications: none recently. Allergies: None known Social: no tobacco, alcohol or recreational drugs use. Physical exam: Vitals: Afebrile, HR 120 and regular, BP 100/70, RR 20 and mildly labored, O2 sat 97% RA Gen: Anxious-appearing female in mild respiratory distress. Skin: Classic urticarial lesions on back, legs and arms. HEENT: Normal. Neck: No adenopathy, thyromegaly, tenderness or swelling. Lungs: Wheezing in all fields with prolonged expiratory phase, no rales. CV: RRR, mild tachycardia, no audible murmurs or rubs. Puerperal pulses present in all extremities, 3 over 4 in intensity. Abdomen: Normal BS, nontender without masses or HSM. Medical decision making: This healthy patient appears to be having an allergic reaction and will need to be observed especially in view of the dyspnea, light headedness at home and soft BP with tachycardia on arrival to the ER. She is awake and alert, has no lip or tongue swelling, but angioedema is in the differential. Working diagnosis: allergic reaction, cause unknown. Differential diagnosis: the cause of hives is broad, hives with wheezing is usually caused by an exposure to an allergen, but other entities or processes must be considered. Such as: Scombroid: Caused by consuming fish containing scombroid (histamine fish poisoning) such as tuna, mackerel, mahi-mahi, and blue fish that are not properly refrigerated. Bacteria in these fish can produce high levels of histamine and thus as allergic type reaction. Serum Sickness: A type 3 (immune complex) hypersensitivity, seen in conditions such as…

Case Based Learning for June 2025

A 53-year-old female with past medical history of type 1 diabetes, asthma, anxiety, and depression, was brought in by EMS with CPR in progress. She called EMS with complaint of difficulty breathing. When EMS arrived, patient was talking and using a nebulizer treatment. Shortly after their arrival, she became unresponsive, apneic, and pulseless. CPR was initiated. An iGel was placed and Lucas chest compression device was placed. On rhythm check, no shock was advised. On arrival to the hospital, SpO2 was 55%, despite bilateral breath sounds and 100% oxygen and adequate bagging. An IV was placed and patient was given Narcan 2 mg, SoluMedrol 125 mg, and magnesium sulfate 2 g IV. She also received epinephrine 0.3 mg IM and a DuoNeb inline.  On rhythm check, sinus tachycardia with a pulse was noted and compressions discontinued. Patient continued to have only agonal respirations. The iGel was removed and she was intubated using etomidate and rocuronium. Her heart rate and blood pressure were increasing and a second dose of etomidate was given while a ketamine infusion was being initiated. EKG showed sinus tachycardia with rate 121 and RBBB. There was also ST depression in the inferior leads and inverted T waves in the lateral leads.  CXR showed ETT in good position 3 cm above the carina and no infiltrates or effusions. Labs: WBC 15.6, H/H 14.2/45.0, plt 322.  INR 1.0, PTT 33.0, dimer 812 (normal 100-599). VBG pH 6.786, pCO2 104, pO2 47, HCO3 15.8, O2 sat 41%. K 5.6, anion gap 23.6. Glucose 399. Trop-I (high sensitivity) 153. After receiving the VBG results, the patient was given bicarb 1 amp. Increased ventilatory rate was used to decrease ETCO2 down to the 40s. Accepting intensivist requested CT head and CTA chest/abd/pel and recommended 2 more amps of bicarb and ceftriaxone be…

Case Based Learning for May 2025

Following is the presentation a patient I recently had in the ED, where I felt I could have done better, especially with documentation. I think it brings up a number of good issues for possible learning/discussion, several of which I’ll mention below. I welcome any thoughts people have. – Gordan Luther, M.D.  HPI: 70 y.o. male, presented for evaluation of a possible stroke. He stated that the prior evening at about 8:00, almost 17 hours prior to his presentation, he had sudden onset of weakness of his left arm and leg. The weakness was severe enough that he had a hard time walking and he feels he had a couple light falls that did not result in injury. He denies any speech or visual change. The same areas have decreased sensation. He had no other complaints. He denied any palpitations, chest pain or SOB. He stated he did not have a history of diabetes despite the blood sugar in the 400s we found on arrival. There was almost no history in the EMR, and he stated he hadn’t seen a doctor for many years. PMH: None other than minor orthopedic injuries No allergies or meds. Lives alone. A friend talked him into coming in for evaluation. VS: BP 202/116 Pulse 102 Temp 36.7 °C Resp 20 SpO2 96% Physical Examination. General: No distress. Cooperative. Appears pale, although nontoxic. Head: Normocephalic. Atraumatic. Eyes: EOMI. PERRL. ENT: No nasal congestion. No pharyngeal erythema or exudate. Mucous membrane moist. Neck: Nontender. Supple. Lungs: Clear bilaterally. No rales, rhonchi, or wheezing. Heart: Regular rate and rhythm. Abdomen: Bowel sounds normal. Soft. Nontender. No rebound or guarding. No palpable masses. Neuro: Alert. Oriented x3. Speech fluent. Cranial nerves 2-12 intact. He has 4 out of 5 muscle strength on the left compared with 5 out…

ERX Community – Making a Difference in Bolivia

  Dr.Gordan Luther, ERx Site Director, recently spent several weeks in Bolivia where he continued a project with Medical Educators for Latin America (MELA). MELA provides trauma courses to Bolivian family doctors and firefighter paramedics. These professionals often handle trauma situations in the field that would typically be managed by paramedics in other countries, so the training is vital. Mano a Mano Bolivia organizes these courses, which have been incredibly well-received, with 50-60 students attending each year. Luther’s work with MELA began after he and his family spent a year volunteering in Cochabamba, Bolivia in 2009. While there, he connected with an NGO called Mano a Mano Bolivia. This NGO builds and maintains clinics and schools in rural areas of Bolivia. They have established over 170 clinics and 60 schools in the last 25 years, all of which remain operational and fully staffed. Inspired by their work, Luther and his family sought to support them upon returning home from that 2009/2010 volunteering year. Luther started taking groups down to Bolivia in about 2015. MELA is now a group of dedicated individuals, roughly half are medical doctors, and the other half firefighter paramedics. To support MELA efforts, the group holds an annual golf tournament fundraiser, and many members contribute personally. The initial goal was to fund one clinic, and now MELA is on their fifth project.  

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