Diagnosis: Acute Pericarditis

Review of the patient's ECG demonstrated diffuse ST-elevations and questionable PR-depression consistent with acute pericarditis. His chest x-ray was interpreted as no acute cardiopulmonary disease. 

The patient's chest exam revealed a faint friction rub. Bedside cardiac ultrasound revealed a mild-to-moderate pericardial effusion. 

The patient's troponin came back at 0.29 and returned to undetectable levels on serial checks. A subsequent formal ECHO study revealed normal cardiac function including normal ejection fraction. 

The patient was admitted to the hospital overnight. His pain improved with oral ibuprofen. A repeat ECG the next day showed resolution of the original ST-elevations and the patient was discharged home with follow-up with his primary care provider. 

Acute Pericarditis

Normally 15-60 cc of physiological fluid between visceral and parietal layers of the pericardium

Inflammatory conditions increase the amount of fluid in this space --> can result in cardiac tamponade depending on the amount of additional fluid and rate at which it increases

Etiologies: viral, idiopathic, post-myocardial (Dresser's syndrome), neoplastic, infectious, uremic, radiation, connective tissue disorders (SLE, RA, Sjogren's syndrome, etc)  

Patient history

• sharp pain of prolonged duration (often days) 
• pleuritic component
• worse when supine
• improved when sitting forward
• prodrome of fever and malaise, not always present but common 

Clinical findings = pericardial friction rub (best heard over left lower sternal border) 

ECG findings

• Stage 1 - diffuse ST-elevations with concave-upwards contour, PR-depressions (most common in II, aVF, V4-6)
• Stage 2 - ST segments become isoelectric and T waves flatten
• Stage 3 - symmetric T wave inversion throughout ECG 
• Stage 4 - normalization 

**PEARL** 

Anything that irritates the outer epicardium of the myocardium will produce ST-elevations. This explains why only transmural infarcts involving the epicardium result in ST-elevation, and why ST-elevations indicate that your pericardiocentesis needle is making contact with the outer myocardium.

Management

• evaluate and treat underlying cause (e.g. dialysis for uremia)
• NSAIDs 

References: 

Colletti JE, Tabas JA, Emergency Medicine: A Focused Review of the Core Curriculum, 1st Ed, 2008, Chapter 2: Cardiovascular Disorders, pages 237-242

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A Little Post-Cold Chest Congestion

A 22 year-old male with history of ventricular septal defect repaired at 2 years of age, and gastritis presents to the emergency department with a chief complaint of chest pain. 

He endorses having a sore throat and other cold symptoms for the past few days that have mostly resolved by now. He reports taking some DayQuil earlier today and later drank a 24 ounce beer. 

A few hours later he started to experience some substernal chest pain described as a constant pressure and occasional burning sensation with mild sweating and shortness of breath. The pain is not relieved by resting or leaning forward. He denies have any associated nausea, vomiting, reflux symptoms, or recent trauma to his chest. 

An ECG  and chest x-ray were obtained and are shown below: 

What is the diagnosis?

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The diagnosis for this case will be posted in approximately 1 week. 

Diagnosis: Spontaneous Pneumothorax

The patient's chest x-ray revealed a right apical pneumothorax estimated 10-15% in size with some mild right basilar atelectasis. No focal consolidation or edema. No acute osseous abnormality.

The pulmonology service was consulted and recommended a period of observation on 100% oxygen. A repeat chest x-ray after 6 hours showed no significant change in size. At discharge the patient continued to endorse pain with deep inspiration, but otherwise reported feeling comfortable. She was given a follow-up appointment with pulmonology for repeat imaging in a week or two.

Pneumothorax

Air between the visceral and parietal pleura

Due to an alveolar-pleural defect between intrapleural space (normally under negative pressure) and the airways (positive pressure)

Defect leads to equalization of pressure until the defect is closed

Simple

• lung collapse on the side of the defect --> decreased lung capacity
• VQ mismatch --> potential hypoxemia depending on size and comorbidities

Tension

• defect acts as a one-way valve --> accumulation of air in the intrapleural space
• mediastinal contents shift away from affected side --> compresses opposite lung
• hypoxia and impaired venous return --> cardiovascular collapse and death

Causes

• Traumatic - blunt or penetrating trauma 
• Iatrogenic - often due to penetrating trauma (i.e. procedure) 
• Spontaneous - no clear precipitating cause
• Primary (no lung disease) = 2/3 cases
• Risk factors: male, smoker, tall, change in ambient pressure, Marfan's
• Secondary (history of lung disease, usually COPD) 
• Risk factors: asthma, cystic fibrosis, lung abscess, TB, interstitial lung disease, malignancy, PJP

Presentation

• sudden onset unilateral chest pain, usually pleuritic, dyspnea, cough
• tachycardia, hyperresonance to percussion, diminished breath sounds

Diagnosis

• clinical suspicion should prompt imaging
• CXR - classically shows pleural line parallel to contour of chest wall with gap of absent lung markings
• CT chest = very sensative
• Grade: small, moderate, large, total

Management

• largely depends on the clinical status of the patient and the size of the pneumothorax

• observation (6 hours) 
• small size pneumothorax <20%
• otherwise young healthy patient
• intrinsic reabsorption 1%-2% per day (increases to 4%-8% on 100% O2)
• may discharge after observation if reliable follow up established for repeat CXR
• simple catheter aspiration 
• moderate size pneumothorax >20%
• less invasive but not always successful
• tube thoracostomy
• most common therapy, especially when more conservative measures fail
• treatment of choice with pleural effusion, respiratory distress, tension pneumothorax
• 20-28 French standard, >28 preferred if pleural fluid present
• water-seal valve (Heimlich or flutter valves) don't require hospitalization
• complications: malposition, infection, pain, obstruction, reexpansion pulmonary edema

management of tension pneumothorax to be discussed in a future post

References: 

Levy SJ, Lex JR, Emergency Medicine: A Focused Review of the Core Curriculum, 1st Ed, 2008, Chapter 4: Thoracic and Respiratory Disorders, pages 237-242

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My Shoulder Really Hurts...

A 27 year-old female presents to the emergency department with chief complaint of right-sided shoulder pain radiating to the chest that started 3 days ago. 

She reports that the pain was initially very severe and exacerbated by every breath on the first day of symptoms. The pain began after waking that morning. The patient went to a local urgent care clinic where she had a shoulder x-ray done that did not show a fracture or dislocation and was discharged with the diagnosis of impingement syndrome. The pain has improved somewhat over the last 2 days but has continues to experience pain with deep inspiration. The pain is also made worse by lying flat.

She denies any recent trauma to her shoulder or chest. She also denies any history of recent long car or plane rides, OCP use, recent surgery, or prior deep venous thrombosis. 

She denies having any shortness of breath, fevers, chills, nausea or vomiting.

Vital signs are within normal limits. The patient appears resting comfortably in bed.

A 2-view chest x-ray was obtained and is shown below: 

What is the diagnosis?

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The diagnosis for this case will be posted in approximately 1 week.

Diagnosis: Pancreatic Adenocarcinoma

CT of the abdomen and pelvis revealed a mass within the pancreatic head and uncinate process, most likely representing pancreatic neoplasm. There was mass effect noted with resultant mild intrahepatic and extrahepatic biliary duct and pancreatic duct dilatation. Also evidence of pancreatitis likely secondary to pancreatic tumor.

The patient's lipase level returned >2400

A subsequent endoscopic retrograde cholangiopancreatography (ERCP) revealed a dilated common bile duct and pancreatic duct but no significant intrahepatic biliary dilation.  With ultrasound a hypoechoic 24 X 23 mm mass was seen in the head of pancreas with upstream dilation of both ducts. Vessels looked clear of the mass. Small amount of ascites noted. Small peritumor lymph node seen.  

Preliminary diagnosis by fine needle aspiration of the mass suggested neoplasm.

Final biopsy results: pancreatic adenocarcinoma.

The patient was discharged on hospital day 3 with follow up with gastroenterology and oncology.

Pancreatic Cancer

Background 

• 4th most common cause of cancer-related death in the United States
• Ductal adenocarcinomas account for 95% of malignant pancreatic tumors
• Pancreatic head involved in 70% of cases
• Especially lethal --> 5-year survival rate < 5%
• Few early symptoms --> most patients diagnosed late 

Risk Factors

• smoking
• advanced age
• high fat diet
• positive family history

Presentation

• constant dull pain in the epigastrium
• weight loss (more due to anorexia than malabsorption) 
• painless jaundice (75% of patients) 
• enlarged palpable painless gallbladder = Courvoisier's sign
• glucose intolerance progressing to diabetes
• migratory inflammatory thrombophlebitis = Trousseau's sign of malignancy

Diagnosis = CT 

Management

• complete resection = only effective treatment
• few tumors (<20%) diagnosed early enough for curative surgical therapy
• complications presenting to the ED
• bowel obstruction
• jaundice
• problems with pain control --> do not withhold narcotics
• consult oncology to address end-of-life issues

References: 

Hemphill RR, Santen SA, Rosen's Emergency Medicine Concepts and Clinical Practice, 8th Ed, 2014, Chapter 91: Disorders of the Pancreas

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Painful Constipation

A 75 year old female is brought in by her daughter for epigastric pain. 

Symptoms were gradual in onset over the last 2 days. She endorses intermittent 8/10 achy discomfort, radiating from her stomach to her lower abdomen. Worse with meals. No associated nausea or vomiting. Last bowel movement was 3 days ago. 

She drinks fiber powder regularly but denies a history of constipation. Her family gave her dulcolax last night. 

On review of systems she has no chills, chest pain, shortness of breath, or dysuria. Her only medical history is hypertension. Surgical history includes hysterectomy and bladder repair. 

On exam her abdomen is soft, mildly tender to palpation over the epigastrium, no rebound or guarding. 

An acute abdominal series was obtained and read as fecal impaction of the cecum and ascending colon without evidence of obstruction.  

A CT abdomen/pelvis with IV contrast was obtained and shown below: 

What is the diagnosis?

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The diagnosis for this case will be posted in approximately 1 week.

Diagnosis: Spontaneous Pneumomediastinum

Review of the patient's CXR was remarkable for evidence of pneumomediastinum and extensive subcutaneous emphysema around the neck. 

A CT chest was subsequently obtained and showed bilateral peribronchial thickening suggestive of bronchiolitis, as well as extensive pneumomediastinum. No evidence of pneumothorax. 

A CT neck was also obtained and showed extensive pneumomediastinum extending into the retropharyngeal space, transverse foramina, and central canal. Extensive subcutaneous emphysema was seen in the in deep soft tissues of the neck, supraclavicular regions, axillae, and left anterior chest wall. 

The patient was diagnosed with viral bronchiolitis producing cough that resulted in spontaneous pneumomediastinum. He was admitted to the cardiothoracic surgery service for observation. A repeat CXR the following morning showed no progression. The patient's chest pain and shortness breath improved over 24 hours. He was discharged the following day with follow-up with his primary care doctor.

Pneumomediastinum

 ***Gas in the mediastinal tissues***

Spontaneous 

• asthma, exertion, Valsalva, seizure, childbirth, intubation, endoscopy, inhaled drugs
• benign clinical course, resolves spontaneously

Secondary

• esophageal perforation, Boerhaave syndrome
• trauma
• pulmonary barotrauma 

Presentation 

• chest pain, dyspnea, throat/neck pain, dysphonia, dysphagia, subcutaneous emphysema in neck and face often with crepitus
• "Hamman's sign or crunch" = crunch sound auscultated with each heartbeat

Complications

• infection, pneumothorax, tension pneumothorax
• mediastinal air in the absence of cardiopulmonary compromise is not life threatening but a cause should be sought

Diagnosis

• Chest x-ray 
• mediastinal air, lucency around cardiac border and aorta
• subcutaneous emphysema
• pneumothorax or other clues as to the cause
• Other tests: Gastrografin or barium swallow, CT, endoscopy

Treatment

• supportive
• search for and manage coexisting conditions 
• airway management if any evidence of respiratory distress or airway compromise 

References: 

Levy SJ, Lex JR, Emergency Medicine: A Focused Review of the Core Curriculum, 1st Ed, 2008, Chapter 4: Thoracic and Respiratory Disorders, pages 236-237

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Pain in the Neck

A 22 year old otherwise healthy male presents to the emergency department with chief complaint of neck pain. He reports having a runny nose, sore throat, and productive cough for the past week that has since improved. Two hours prior to arrival he says the skin over his neck began to feel painful to touch, worsened by coughing and swallowing. Also endorses associated feeling of "warmth." 

On review of systems he endorses mild shortness of breath and chest pressure. He denies nausea, vomiting, diarrhea, headache, or rash.

A chest x-ray with PA and lateral views was obtained and is shown below: 

What is the diagnosis?

How would you manage this patient? 

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The diagnosis for this case will be posted in approximately 1 week.

Diagnosis: Acute Appendicitis

CT scan of the patient's abdomen and pelvis revealed a 1.2 cm dilated appendix with adjacent stranding consistent with acute appendicitis without perforation or abscess. Also noted was mild dilatation of the terminal ileum likely representing focal ileus. 

General surgery was consulted. Intravenous Cefazolin was ordered. The patient was taken to the operating room within the hour. 

Acute Appendicitis

Background

• most common abdominal surgical emergency in the United States
• caused by obstruction (appendecolith, foreign material, adhesions, etc) 
• may occur as result of lymphoid hyperplasia after viral infection
• highest incidence in ages 10 - 30 
• Hightest misdiagnosis rate in extremes of age (infants and elderly) 

Presentation

• pain initially vague and poorly localized in periumbilical region with nausea, anorexia and fever
• subsequent RLQ pain over next 24 hours as peritonitis develops
• atypical presentations:
• RUQ pain (pregnant patients) 
• right lower back pain (retrocecal appendix) 
• pelvic/adnexal pain (appendix near ovary) 
• dysuria (appendix near bladder) 
• diagnosis commonly delayed in infants and elderly due to atypical presentation and results in perforation rates >50% in these groups

Diagnosis

• primarily clinical 
• leukocytosis in 80% of cases 
• CT scan has >90% sensitivity and specificity 
• ultrasound is not as sensitive or specificity but is imaging modality of choice for children and pregnant women 

Treatment

• early surgical consultation
• antibiotics 
• surgery

References: 

Martinez JP, Mattu A, Palmer G, Emergency Medicine: A Focused Review of the Core Curriculum, 1st Ed, 2008, Chapter 3: Abdominal and Gastrointestinal Disorders, pages 205-206

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Abdominal Pain and Diarrhea

An 18 year-old female presents to the emergency department with abdominal pain and diarrhea. She describes a gradual onset of sharp pain in her lower abdomen this morning that has progressively worsened with associated fever, chills, nausea and anorexia. She also reports having 3 watery bowel movements today without any blood or melena. 

A CT scan of the patient's abdomen and pelvis is shown below: 

What is the diagnosis?

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The diagnosis for this case will be posted in approximately 1 week.

Diagnosis: Acute Anterior STEMI

The patient's ECG revealed grossly elevated ST segments in anterior leads including "tombstone T-waves" consistent with diagnosis of acute anterior ST-segment elevation myocardial infarction. The Cath Lab was immediately activated by the ED and the patient started on a heparin drip after negative FOBT. 

In the Cath Lab the patient was found to have 100% stenosis of the proximal left anterior descending (LAD) artery, 80% stenosis of the mid LAD artery, and 70% stenosis of the proximal right coronary artery (RCA). A stent was placed in the LAD reducing the occlusion to 0% stenosis. The patent's left ventricular ejection fracture post-procedure was 35-40%. 

The patient expired 2 days later in the Cardiac Intensive Care Unit secondary to respiratory complications.

In the ECG below, note that there are ST-segment elevations in leads V1 through V6 and slight elevation in lead I suggesting septal (V1-V2), anterior (V3-V4) and lateral (V5-V6, I) wall involvement, as well as reciprocal changes in the inferior wall leads (II, III, aVF) 

ED Management of Acute STEMI

Why we care? 

• Acute coronary syndromes are a leading cause of death in adults in many developed countries 

Quick Pathophys Review

• Coronary blood flow fails to meet myocardial O2 demand --> ischemia/infarction

• Most coronary stenosis preceding an acute MI is <50% - the problem is acute plaque rupture

• Acute plaque rupture --> platelet activation --> thrombus formation --> acute total occlusion --> exacerbated by subsequent vasospasm

• Further damage due to reperfusion injury secondary to oxygen free radicals, calcium, and neutrophils

ED Management

• Primary goal = early coronary patency and revascularization 
• primary angioplasty vs fibrinolysis 
• treatment within first 1-2 hours of event confers substantial benefit 

• Management goals for ED provider: IV, O2, Monitor
• early recognition (history, physical, ECG) 
• early activation of hospital "STEMI system" and cardiology consult
• early pharmacological therapy

• Nitroglycerin (0.4 mg or 400 ug sublingual) 
• reduce preload --> reduce myocardial O2 demand --> pain relief 
• reduces afterload to lesser extent
• thought to increase myocardial perfusion by increasing collateral coronary flow
• mostly provides pain relief, no significant mortality benefit identified
• CAUTION in preload-dependent states:
• inferior wall MI
• right ventricular infarction
• sudden drop in preload may cause profound hypotension

• Morphine (2-5 mg IV q5-30 min)
• additional pain relief agent when symptoms refractory to nitroglycerin 
• pain relief and anxiolysis reduce O2 consumption and myocardial work
• some preload reduction as well
• CAUTION in hypotensive patients as can further reduce BP

• Aspirin (160-325 mg po)
• large RCTs have demonstrated as much as a 25-50% reduction in mortality
• irreversibly inhibits platelet cyclooxygenase --> block thromboxane A2 enzyme production (platelet aggregator) --> reduced thrombus formation

• Heparin (80 units/kg bolus, 18 units/kg drip)
• strong synergistic effect with aspirin in preventing death from acute MI 
• activates antithrombin III --> inactivates Factors II and X --> prevent conversion of fibrinogen to fibrin --> inhibits clot propagation (no clot lysis) 
• CAUTION in patients with any signs, symptoms or history of bleeding
• always perform FOBT before administering 

• Fibrinolytic therapy - tPA, Streptokinase 
• activates intrinsic tissue plasminogen enzyme --> dissolves thrombus
• ACC/AHA Level I Recommendation in acute MI
• The Good
• well-studied
• improves coronary flow
• limits infarct size
• improves survival in acute MI
• The Bad
• numerous relative and absolute contraindications limit its use
• high risk for bleeding complications including intracranial hemorrhage

• Percutaneous coronary intervention (PCI)
• mechanical clot disruption by endovascular instrumentation under fluoroscopy
• increased number of eligible patients
• lower risk for intracranial bleeding
• significantly higher reperfusion rate 
• earlier characterization of coronary anatomy to guide surgical intervention
• risk stratification allowing early and safe hospital discharge 

Disposition = Cath Lab

• studies suggest <90 minute door-to-ballon time necessary for optimal myocardial salvage
• Time = Myocardium!

References: 

Kurz MC, Mattu A, Brady WJ, Rosen's Emergency Medicine Concepts and Clinical Practice, 8th Ed, 2014, Chapter 78: Acute Coronary Syndrome

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Gnawing Discomfort

An 82 year-old male with history of hypertension presents to the emergency department in the early morning for insomnia. He reports being awoken approximately 6 hours prior to arrival by a 2/10 "squeezing" pressure in his right chest that came on insidiously. The pressure has been constant since onset, is non-radiating, and associated with shortness of breath. The patient denies having any pain and describes his symptoms as rather a "gnawing discomfort." He reports feeling well the night before and denies having symptoms like this in the past. He denies any personal or family history of heart or lung disease. On review of systems he denies having nausea, vomiting, cough, fever, or chills. 

Vital signs T 37.5 | P 102| 146/73 | 20 | 100% on RA
On exam the patient is an elderly male in minimal distress sitting upright in bed. 
Heart sounds are rapid and regular with no murmurs or gallops.
Breath sounds are clear bilaterally.

An electrocardiogram is obtained and shown below:

What is the diagnosis?

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The diagnosis for this case will be posted in approximately 1 week.

Diagnosis: Hypertensive Intracerebral Hemorrhage

A CT scan of the patient's head revealed a left basal ganglia hemorrhage with intraventricular extension causing midline shift due to early cerebral edema. 

Soon after viewing the CT scan findings the patient began to develop bilateral extensor posturing. Pupils continued to be equal and reactive. A dose of IV mannitol was delivered followed by intubation after pre-medication with IV lidocaine. The patient was hyperventilated to a goal PCO2 <35. Neurosurgery was consulted for emergent placement of an endoventricular device and the patient admitted to the neurological intensive care unit.

Subsequent CT angiogram of the patient's head revealed no evidence of an aneurysm or arteriovenous malformation. A urine toxicology screen was negative for cocaine or methamphetamine. Neurosurgery ultimately diagnosed the patient with a hypertensive intracerebral hemorrhage. It was later learned from the patient's family that she had a history of poorly controlled hypertension, hepatitis C, and regular IV heroin use for the past 5 years. 

ED MANAGEMENT OF ELEVATED INTRACRANIAL PRESSURE (ICP)

RAPID FIRE

Why we care

• Increased ICP --> cerebral herniation --> permanent disability and/or death

Intubation (patient is obtunded, not protecting airway, GCS <8) 

• Perform brief neuro exam before sedating/paralyzing
• Lidocaine 1.5-2 mg/kg IV push
• thought to blunt the increase in ICP due to stimulation of patient's airway 
• controversial, limited data/evidence to back efficacy
• Induction agent = Etomidate
• minimal cardiopulmonary disturbance = minimal ICP disturbance
• Paralytic agent = Succinylcholine (barring obvious contraindications)
• good for rapid onset
• some sources recommend pre-medicating with sub-paralytic dose of a nondepolarizing agent to mitigate fascinations and possible increase in ICP

Hyperventilation

• Goal is to reduce PCO2 to range of 30 - 35 mmHg 
• increases cerebral vasoconstriction --> reduced cerebral blood flow
• onset of effect in 30 sec, peak effect at 8 min
• thought to lower ICP by as much as 25% 

Osmotic Agents

• Mannitol (0.25-1 g/kg) = mainstay 
• reduces cerebral edema by osmotic gradient pulling water out of cells
• effect occurs within minutes; peak effect at 60 min
• lasts 6-8 hours
• Pros
• expands blood volume helping maintain systemic pressure
• promotes cerebral blood flow by reducing blood viscosity 
• free radical scavenger
• Cons 
• hypotension and renal failure in large doses
• increased bleeding into traumatic lesions by reducing hematoma tamponade

• Hypertonic Saline 
• used for increased ICP since 1919
• significantly reduces ICP
• encouraging data showing benefit of continuous infusion of 3% HTS in pediatrics
• Cons
• conflicting data regarding efficacy
• renal failure
• central pontine myelinolysis
• rebound increase in ICP

• Steroids do not lower ICP, some studies even suggest increased mortality

Emergent Neurosurgical Consult

• If patient not responding to above measures then may likely require:
• emergency burr holes (epidural hematoma)
• decompressive craniectomy (epidural hematoma) 
• endoventricular device (expanding intraventricular hemorrhage)

References: 

Heegaard WG, Biros MH, Rosen's Emergency Medicine Concepts and Clinical Practice, 8th Ed, 2014, Chapter 41: Head Injury

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