Case of the Week COW#16

Posted on by Yenis Paez-Perez

CC: BIB BLS for “Psych Evaluation”

HPI: 46-year-old female w/ PMH of asthma, SLE, RA and seizure disorder presents to the emergency department by BLS for evaluation. Patient states, “I don’t like people accusing me of doing things I didn’t do, I only took 2 Percocet and that’s it!” Patient states that she has been feeling depressed and “everything I do is never good enough for my kids, I buy them car, and I don’t even have car myself.” Patient appears to have multiple scratches over her face and left wrist, but is not willing to elaborate how she sustained them or provide any additional history. Denies any suicidal ideations, homicidal ideations, or hallucinations. There is no known psychiatric history.

Per family and EMS, patient was in her bedroom with the door shut, “not acting right, she was asking for us to pass her the key under the door to get out of the room but there is no lock on the door. She did this once before but it went away, today is more severe.” Pt was found in her bedroom by EMS with 2 empty beer cans and bottles of Percocet nearby. She had a recent URI for which she was taking Zzz-quil.

Medications: oxycotin 60mg q12h prn, Percocet 10/325mg q4-6h prn, toradol 10mg TID, ambien CR 12.5mg qHS, ProAir HFA 2 puffs q6h, Zzz-quil

 Physical Exam:

VS: 148/101, HR 111, RR 18, T 99.1, SpO2 95% on RA
General: Awake, alert, coherent, intermittently tearful
HEENT: superficial abrasions over face, otherwise NCAT; moist mucous membranes
Eyes: 3mm PERRL
Cardiac: tachycardic, regular rhythm, no M/R/G
Lungs: CTA b/l
Abd: soft, NT, ND, normal active bowel sounds
Neuro: AAOx3, lucid, following commands, moving all 4 extremities, no gross deficits, steady gait w/o difficulty
Skin: multiple superficial abrasions over face and L wrist, normal moisture
Extremities: 2+ distal pulses, warm, normal color
Psych: Anxious appearing, depressed mood, emotionally labile, intermittently tearful; denies SI/HI

Pertinent Labs (if any)
CBC: 11.7>16.5/50.1<324
CMP (@15:09 hours): Na 135, K 4.6, Cl 106, CO2 5, Glucose 132, BUN 9, Cr 0.98, GFR >60
Alk phosphate 77, AST 59, ALT 66
UA: Moderate blood, 0-3 RBCs, occasional calcium oxalate crystals, otherwise WNL
Alcohol: <10 mg/dl
UDS: (+) cocaine
Acetaminophen: <10.0 ug/ml
Salicylate: <2.5 mg/dl
Repeat CMP (@ 17:30 hours): Na 138, K 5.4, Cl 109, CO2 <2, Glucose 143, BUN 9, Cr 1.10 GFR:53, Alk phos 77, AST 69, ALT 74
Serum Osmolality: 334 mOsm/kg (N: 283-299)
Calculated osmolar gap: 53.0 mOsm/kg
ABG: pH 7.00 / pCO2 13 / pO2 151 / HCO3 – 3.2
ABG Lactate: 20.0 mmol/L
Serum lactic acid: 1.2 mmol/L
Acetone: Negative

ECG in the ED

Working Diagnosis: Anion gap metabolic acidosis, most likely due to ethylene glycol poisoning

ED/Hospital course:  In the ED patient became increasingly altered. Upon arrival patient was coherent, AAOx3, tearful. Upon reevaluation she was found in room shaking back and forth talking to herself and banging her hands on the bed rails, more confused, inappropriate in her thoughts and actions. A short time later she was found on the floor next to stretcher and was AAOx1, agitated, combative, not following commands, fighting with staff, incontinent of urine. Lab results returned at this time and the patient was subsequently intubated, received 1 amp sodium bicarbonate prior to intubation and admitted to MICU. Repeat labs in MICU showed persistent anion gap metabolic acidosis with Bicarbonate of 5 and anion gap of 26. She was placed on bicarbonate drip and received emergent HD. After HD, the acidosis improved with a bicarbonate value of 19 afterwards. Additionally placed on fomepizole. Received 2 rounds of HD. Subsequently extubated and transferred to floor. Upon extubation she continued to deny any SI or toxic ingestion. Methanol and ethylene glycol levels (-), however, they were drawn after HD was performed.

 Pearls: Brief differential diagnosis of anion gap metabolic acidosis:

  • Methanol, metformin
  • Uremia
  • Diabetic or alcoholic ketoacidosis
  • Paraldehyde
  • Isoniazid, Iron, Inhalants (carbon monoxide, cyanide, hydrogen sulfide)
  • Lactic acid
  • Ethylene glycol (ethanol may produce a small gap)
  • Salicylates, solvents

Osmolar gap:

  • Calculated osmolar gap ≥10 is consistent with poisoning by alcohols (ethanol, methanol, ethylene glycol, isopropanol, propylene glycol), glycerol or mannitol
  •  Absence of osmolar gap does not exclude toxic alcohol poisoning.
  • Normal osmolar gap: ±10
  • Normal serum osmolality: 280-295 mOsm
  • Osmolar gap formula: (2 x Na) + BUN/2.8 + Glucose/18 + Ethanol/4.6
  • Labs for this calculation (i.e. serum osmolality, ethanol, and SMA-7) must be drawn at the same time for accuracy

Toxic Alcohol Poisonings:

  1. Methanol
  • Found in windshield washing fluids, solvents, paint thinners and canned fuels
  • Converted by alcohol dehydrogenase to formaldehyde then to formic acid
  • Accumulation of formic acid correlates with the decrease in bicarbonate, the increase in anion gap, and the severity of the metabolic acidosis
  • Formic acid affects optic nerve function, causing optic papillitis and retinal edemaà “blind drunk”
  • Visual symptoms include photophobia, “snowstorm” vision, and blindness
    • Management:
      • Supportive measures including airway management
      • Severe acidosis is treated with bicarbonate to reduce diffusion of formate into the CNS and protect the optic nerve
      • Alcohol dehydrogenase inhibitor (ethanol or fomepizole) to block further metabolism of methanol
      • Fomepizole Fomepizole (4-methylpyrazole) is preferred iv.
      • Hemodialysis to remove methanol and formic acid indicated if methanol level >50 mg/dL, metabolic acidosis (arterial pH ≤ 7.25), severe visual or CNS symptoms
  1. Ethylene glycol
  • Found in antifreeze and brake fluids
  • Converted by alcohol dehydrogenase to glycolaldehyde which is metabolized to glycolic acid
  • Glycolic acid is primarily responsible for the anion gap metabolic acidosis; it is metabolized to multiple metabolites including oxalic acid
  • Oxalic acid forms calcium oxalate crystals in the kidney, brain and liver
  • Initial CNS changes suggestive of ethanol intoxication progressing over 9-12 hours to possible seizures, stupor, coma; toxicity may progress to pulmonary edema and myocardial dysfunction
  • Late toxicity is characterized by renal failure
  • Positive birefringent calcium oxalate crystals in the urine; often absent initially commonly described as “envelope-shaped”
  • May see hypocalcemia although not always present
  • Management:
    • Alcohol dehydrogenase inhibitors: Fomepizole or ethanol
    • Hemodialysis with same indications as methanol above
    • Thiamine and pyridoxine can be administered to decrease production of oxalic acid
    1. Isopropanol
  • Isopropyl (rubbing) alcohol
  • More intoxication/CNS depression but generally less severe sequlae than methanol and ethylene glycol 80% is absorbed from the stomach within 30 minutes and metabolized by alcohol dehydrogenase to acetone
  • Presentation: CNS depression, hypotension in severe cases, hemorrhagic gastritis/tracheobronchitis
  • Positive serum acetone and acetonuria
  • Anion gap metabolic acidosis is generally not a feature of isopropanol toxicity (unless you have significant hypotension with subsequent lactic acidosis)
  • Management:
    • Supportive care, including airway management
    • Alcohol dehydrogenase inhibitors are not indicated
    • Hemodialysis indicated for refractory hypotension or serum levels >400-500 mg/dL

Some Additional Points:

      • Lactic acid on lab analysis may be falsely elevated and vary depending on how the sample is analyzed. You will note that ABG lactic acid and serum lactic acid analyzed by lab are very different values, this is due to the fact that a metabolite of ethylene glycol’s metabolism has a very similar chemical structure to lactic acid, causing a falsely positive elevated lactic acid
      • The differential diagnosis of anion gap metabolic acidosis listed above is a limited list of the most commonly noted causes of AG metabolic acidosis; a comprehensive list is much broader
      • An osmolar gap >50 is highly suggestive of toxic alcohol ingestion; a level >100 is virtually pathognomonic—there is really nothing else that can cause such a severely elevated osmolar gap other than toxic alcohol

Case presented by Dr. GregnCassidy

Special thanks to Dr. Kashani for his guidance in preparing this case.

Case of the week COW #15

Posted on by Yenis Paez-Perez

CC: Shortness of breath

HPI: 7 day old female presents to the Emergency Dept. (ED) after being seen earlier in clinic. Mother is rom Nigeria and arrived to the U.S a few weeks prior to delivery. Prenatal care is unclear. Patient was delivered via C-Section at 39 weeks at another nearby hospital. Both mother and baby spent one day in the hospital after delivery being discharged home. Mother states that since last night, the baby appears to “ not breathing right.” She also hasn’t’ been eating much and is crying more often than usual, during which her lips start to turn blue.

Physical Exam:
Obvious respiratory distress, hypoxic on RA, saturating in the middle to low 80’s on NC 3 L
HR 176,   RR 60.    Accuchek 96.
BP: (RA) 69/45    BP (LA) 91/64     BP (LL) 84/64     BP (RL) 71/58

Pertinent Imaging/ECG

ECG in the ED:

Working Diagnosis: Shock secondary to congenital cardiac pathology.

ED/Hospital course:  Patient was admitted to PICU, underwent Echocardiogram and further imaging and was diagnosed with Coarctation of the Aorta. The patient was transferred to Mt. Sinai for operative repair.

Pearls:

  • 7 day olds are terrifying, especially if they are sick.
  • Take a breath! Start with your ABCs.
  • Coarctation of Aorta(CoA) is a congenital aortic narrowing which most commonly occurs at the level of ductus arteriosis. There are Pre-ductal and Post-ductal types. Pre-Ductal CoA is a Truncus dependent lesion and most patients present within 2 weeks of birth once duct closes. Aortic narrowing leads to increased LV function and dilation. Post-ductal are commonly identified in adulthood.
  • Obtain a BP/pulse Ox in all 4 extremities
  • Perform the Hyperoxia test
    • Obtain ABG on RA. Then, apply 100% supplemental oxygen with a NRB for 10-15 minutes. Repeat the ABG on the NRB.
      • On repeat ABG
        If PaO2 > 250mmHg = Lung problem
        If PaO2 < 100mmHg = Congenital Heart Disease
        If PaO2 100-250: Assume the worst situation first
  • You may also apply supplemental oxygen and assess the infant’s response. If saturation increases to at least 5-10%, it’s most likely a Lung problem. If it remains the same, think about Congenital Heart Disease
  • Prostaglandin (pt is less than 4 weeks old typically 1-2 weeks of life) start at 0.05 mcg/kg/min.
  • Dr. Hochman rule #11, call consultants early “don’t be the captain of a sinking ship”
  • Additional medications: Lasix 1 mg/kg if evidence of volume overload.Ductal dependent lesions, pulmonary presentation cyanosis/hypoxia use phenylephrine . If systemic SX, shock, pulmonary congestion on CXR Milrinone (decrease afterload + inotropic support).

The SICK NEONATE!

Case presented by Dr. Daniel Poor

Pediatric Pneumonia

Posted on by Yenis Paez-Perez

 3-year-old boy presents to the ED with a 4-day history of cough and 1-day history of fever. Per family patient has been having rigors and chills with vomiting. He also reports chest pain with coughing. His immunizations are UTD. The child does not appear toxic,

VS: Temp 103.3F,  BP 90/65,  HR 100,  RR 30,  96% O2 Saturation on RA.
Patient has some intercostal retractions, with decreased air entry on the right side with audible crackles.

Questions for EM physician

  • How do you make the diagnosis of pneumonia?
  • Distinguishing patients with bacterial pneumonia, who would benefit from antibiotics, from those with nonbacterial pneumonia who would not.
  • Who requires inpatient management vs. patients that can be safely discharged home on oral antibiotics.
  • Pneumonia is the number 1 killer of children worldwide.
  • Pneumonia occurs more often in early childhood than at any other age and causes significant morbidity and mortality.
  • Identifying the cause of pneumonia in children is difficult due to a lack of rapid, accurate, commercially available laboratory tests for most pathogens. Empirical therapy based on patient’s age, clinical scenario and risk factor is the most common course in most cases.
 Age-specific causes of pneumonia in otherwise healthy children. Pathogen listed in order of frequency
Neonates GBS, E. Coli, Listeria Monocytogenes, Staphylococcus
1 month – 2 years RSV, Parainfluenza virus, Metapneumovirus, Influenza virus, Adenovirus, S. Pneumoniae

 **3 weeks to 3 months of age (Pneumonitis syndrome/Afebrile Pneumonia Syndrome (APS))*: Chlamydia trachomatis, RSV, Parainfluenza virus, Bordetella pertussis
2 – 5 years RSV, S. Pneumoniae, Non-typeable H. Influenzae (NTHi), Group A Streptococcus, Mycoplasma pneumonia, Chlamydia pneumonia
6 – 18 years Mycoplasma pneumonia, Chlamydophila pneumonia, Streptococcus pneumonia, NTHi, Influza virus A , other respiratory viruses
  *Infants (1 – 3 months of age) may present with a characteristic syndrome of cough, tachypnea, progressive respiratory distress, and radiographic evidence of bilateral diffuse pulmonary infiltrates with air trapping. Most are afebrile. This syndrome is also called APS. The most common pathogen included Chlamydia trachomatis and respiratory viruses. Infection of Bordetella pertussis should also be considered due to recent dec. in immunization. Acutely, APS is generally benign and self-limiting disease. In such cases, infants often have viral illness, which does not respond to antibiotic therapy, but differentiating bacterial from viral illness is often difficult. Consider empiric antibiotic therapy.

Diagnosis of pneumonia:

    • Definition: Essentially it is infection of lower respiratory tract in the presence of radiographic abnormalities on CXR.
    • WHO guidelines for pneumonia in children is cough and tachypnea
      • Age < 2 months: Tachypnea is >60 RR
      • Age 2 months to 5 months: Tachypnea is >50 RR
      • Age >12 months: Tachypnea is > 40 RR
    • Clinical features
      • Fever and tachypnea are sensitive but not specific
      • Cough
      • Productive cough is rarely seen before late childhood
      • Consider pneumonia in any child presenting with prolonged fever, prolonged cough, high fever, as well as focal respiratory findings not including wheezing, especially with the presence of multiple symptoms.

Evaluation
Absence of tachypnea, respiratory distress, and rales/decreased breath sound rules-out pneumonia with 100% sensitivity

  • CXR: Cannot differentiate between viral and bacterial (but lobar infiltrate more often bacterial)
      • Consider for:
        • Age 0-3mo (as part of sepsis work up)
        • <5yr with temperature >102.2, WBC >20K and no clear source of infection
        • Ambiguous clinical findings
        • Pneumonia that is prolonged or not responsive to antibiotics
    • Consider RSV, Influenza 

Treatment

 Empiric Antimicrobial Therapy For Children with Pneumonia by Age group
Age group Outpatient Inpatient
Neonates NOT RECOMMENDED Ampicillin 200 mg/kg/d IV divided Q6H

+ Gentamycin 7.5 mg/kg/d IV divided Q8H

OR

+ Cefotaxime 150mg/kg/day IV divided Q8H

Consider Cloxacillin and Nafcillin for patient with S. aureus infection or Vancomycin for MRSA
3 wk – 3 mo NOT RECOMMENDED Azithromycin 10 mg/kg IV first dose, then 5 mg/kg IV QD for 4 days

 
3 mo – 5 yr* Amoxicillin 80 – 100mg/kg/day in 2 divided doses Ampicillin 200 mg/kg/d IV divided Q6H

OR

Ceftriaxone 50 mg/kg Q24hrs

Consider Azithromycin 10 mg/kg IV first dose, then 5 mg/kg IV QD for 4 days

Consider Vancomycin for seriously ill patients
6yr – 18yr* Azithromycin 10 mg/kg for first dose, then 5 mg/kg daily for 4 days Azithromycin 10 mg/kg IV first dose, then 5 mg/kg IV QD for 4 days

PLUS

Ceftriaxone 50 mg/kg Q24hrs

Consider Vancomycin for seriously ill patients
*Refer to AAP guideline on management of pediatric pneumonia below

Disposition

  • Consider Admission For
    • Age: <2-3 months old (Consider up to 6 months)
    • History of severe or relevant congenital disorders (Cystic fibrosis)
    • Suspected complication (Empyema)
    • Vomiting, dehydration, unable to tolerate PO
    • Immune suppression (HIV, SCD, malignancy)
    • Toxic appearance/respiratory distress
    • SpO2 <90-93%
    • Social circumstances

Post by Dr. Michael Hong

Case of the Week COW#13

Posted on by Yenis Paez-Perez

CC: Chest Pain

HPI: 49-year-old female brought in via ALS presents complaining of Chest pain. As per the Paramedics, the patient was found to be in no acute distress, stating she had exertional chest pain, which had subsided. The pre-hospital ECG was suspicious for ischemia and she was given ASA. Patient states she was walking home from the store when she began to have a pressure like pain on the left side of her chest, which was non-radiating and persisted when she laid down. She admits to feeling similar symptoms over the past few months, but today was the most severe. Upon arrival to Emergency Department, she denied chest pain, SOB, palpitations, abdominal pain, nausea or vomiting. Denied ETOH or illicit drugs use

 Physical Exam:
BP:128/91, Hr:88, RR: 14, Temp: 98.0, Pulse O2: 100% RA
General: Patient lying comfortably in bed, in no distress
HEENT: NCAT, pupils PERRLA, neck supple
Respiratory: non-labored, CTA B/L, no wheezing, rales or rhonchi
Cardiac: +S1/S2, no MRG, regular rate and rhythm
Abdomen: soft NT ND, + BS
Neuro exam: AAO X 3, lucid, strength is 5/5 in all extremities, muscle tone is intact,
Skin: No rash or peripheral edema.

Pertinent Labs:
CBC: Unremarkable
CMP: Unremarkable
Troponin: Negative (< 0.010)

Pertinent Imaging/ECG
CXR: no acute infiltrate, No Pneumothorax or cardiomegaly. Normal Chest X-ray
Pre-Hospital ECG

ECG in the ED

Working Diagnosis: Left Main Insufficiency

ED Course: Repeat ECG in ED showed NSR and had completely normalized. Case was discussed with Interventional cardiologist on call. A Code STEMI was activated and patient was taken emergently to the Cath lab. She was given a Heparin bolus as well as Plavix.

ED/Hospital course:  The catheterization report revealed 80-90% Distal left main, 30 % mid LAD, and LM stenosis improved partially during catheterization with nitroglycerin. Patient admitted to recently using cocaine. CT surgery was called due to the fact that patient had recent cocaine use and it was believed she might have had Left Main Coronary spasm. On hospital day 2, patient went back for repeat catheterization, which revealed Left main distal 30% and LAD mid 30% stenosis. Patient was transferred to telemetry, and discharged on hospital day 4.

Pearls:

aVR in ACS
Typical ECG findings with left main coronary artery (LMCA) occlusion:

  1. Widespread horizontal ST depression, most prominent in Leads I, II and V4-6
  2. ST elevation in aVR ≥ 1mm
  3. ST elevation in aVR ≥ V1

(Don’t worry so much about STE 0.5mm or less in lead aVR, because it lacks specificity. Using 1.0mm or greater in lead aVR, has better specificity)

ST-Segment Elevation in lead aVR foreshadows a worse prognosis in ACS and often predicts the need for CABG. Patients with NSTEMI and ST elevation ≥ 1mm in aVR are likely to have multi-vessel or LMCA disease and are likely to require CABG, therefore withholding Clopidogrel may be prudent. ST-segment elevation in aVR can be caused by any of the following 4 mechanisms

  1. Critical narrowing of the LMCA causing sub-endocardial ischemia due to insufficient blood flow. (LMCA insufficiency)
  2. Transmural infarction of the basal septum due to a very proximal LAD occlusion or complete LMCA occlusion (patient will be VERY sick)
  3. Severe multi-vessel coronary artery disease.
  4. Diffuse sub-endocardial ischemia from oxygen supply/demand mismatch.

Patients with complete occlusion of the LMCA (mechanism 2), often present in cardiogenic shock and require immediate revascularization. Patients with acute coronary occlusions typically will have active symptoms and look sick!

There is an estimated 70% mortality without immediate PCI. Medical therapy (including thrombolytic) does not improve mortality. Emergency PCI may decrease mortality to 40%.

 What Else can Cause STE in aVR that Won’t Benefit from Going to the Cath Lab?

Other causes of global cardiac ischemia
o Thoracic aortic dissection
o Large pulmonary embolism
o Severe anemia
o Post-arrest (within 15 min. of epinephrine or defibrillation)

oMiscellaneous causes
o Supraventricular Tachycardia (esp. AVRT)
o Left bundle branch block (LBBB) & paced rhythms
o LVH with strain (from severe hypertension)
o Severe hypokalemia
o Na+ channel blockade (TCA toxicity, hyperkalemia, Brugada, etc.)

REMEMBER: ST-Segment Elevation in Lead aVR is NOT SPECIFIC for an acute LMCA Lesion, Acute Proximal LAD Lesion, or Acute Triple Vessel DiseasE

    • Correlate Your ECG with the Patient’s Clinical Status
    • Patients with ACS due to LMCA Blockage, Triple Vessel Disease, or Proximal LAD blockage will look “sick” due to global cardiac ischemia

Case presented by Dr. Kerri Clayton.

Case of the Week COW #12

Posted on by Yenis Paez-Perez

CC: Left leg pain

HPI: 52 year old male with PMH of IDDM presents to the Emergency Dept. (ED) with left leg pain for the past 9 days which has become progressively worse. He is a taxi driver and reports that a part of the seat, which supports his legs, has been rubbing against his left hip/buttock/thigh and he thinks this is what’s causing the pain. He reports pain to the back of his left buttock, which radiates down the leg “like a shooting pain.” The patient has been to the ED multiple times already for similar complaints, requesting for stronger pain medications. He is upset because he feels the medicine just isn’t working. At this point, the patient is uncooperative and refuses to answer any more questions. Further history was obtained from his previous visit history, which stated he was discharged yesterday with a diagnosis of sciatica and a prescription for Lidoderm patch, Motrin and Percocet.

PMH/Birth History: N/A

Social History: N/A, refused to answer any further questions

PHYSICAL EXAM

VS: BP 125/59     HR 108     RR18   T: 98F   98% RA

General: In moderate acute distress, appears stated age, in moderate pain, uncomfortable and diaphoretic.

HEENT: Atraumatic, normo-cephalic. No deformities. PEERLA

Respiratory: Lungs CTA bilaterally.

Cardiac: +S1/S2, no MRG, regular rate and rhythm

Abdomen: soft NT ND

Extremities: B/L DP 2+, Cap refill < 3 seconds, positive straight leg (LLE); pain isolated to (L) buttock and posterior lateral thigh.

Neuro exam: CN III –XII intact. 5/5 strength in all 4 extremities with limited ROM in the LLE secondary to pain.

Skin: Diffuse erythema over the Left buttock extending down to the posterior lateral left thigh, with pitting edema. No fluctuance or streaking noted.

Labs:

WBC: 24.7     H/H: 13.1 / 39.4     Platelets 245     PMH: 22.1  Lymph: 0.7     Mono: 1.5

Na: 126     K: 5.5                 Cl: 89       CO2: 22           Glucose: 438

Bun: 38     Cr: 1.17         Alk P: 140       LFT: WNL         Albumin 3.2

Acetone: NEG

ESR: 65

CRP: 30

Lactic acid: 1.4

Images:

Repeat Vital Signs 139/81   89   16     99.7F   97% ON RA

MRI

 

 

Working Differential Diagnosis: Pyomyositis

ED/Hospital course:  Orthopedic Surgery was consulted. X-Ray did not show obvious bony involvement and ESR/CRP was not suggestive of osteomyelitis. MRI was performed on the LLE, which sowed a hyper-intense signal within multiple muscles of the pelvis and left thigh consistent with myositis. Collection within the Obturator Externus and Gluteus Maximus muscles likely represented an abscess consistent with pyomyositis. The patient was started on Vancomycin and Zosyn and sent to Interventional Radiology for drainage of the abscess. The cultures grew back MSSA. The left knee tap did not grow any organisms on Gram Stain. IR drainage was followed by orthopedic washout and debridement of the musculature with insertion of JP drain for continuous drainage. The patient’s antibiotics were switched to Levaquin and he was subsequently discharged home with Clindamycin and Bactrim for 2 more weeks. He tested negative for HIV.

Pearls & Takeaways:

  1. Don’t blow off patient’s complaints! Our patient presented with History and Physical exam consistent with sciatica with a positive straight leg test. He was on Percocet and kept asking for stronger medications for his previously diagnosed Sciatica.
  2. Make sure to undress the patient and examine the skin!
  3. If the patient is complaining of pain out of proportion to his/her exam, dig a little deeper for alternative differential!
  4. Since his Accucheck was High, further laboratory testing was done which revealed leukocytosis. The elevated white count prompted me to perform a further work up
  5. Always re-evaluate the patient! On re-evaluation, he appeared sicker and with cool, damp skin on his back and neck, solidifying my gestalt that maybe I am missing something
  6. Pyomyositis is a purulent infection of skeletal muscle that arises from hematogenous spread, usually with abscess formation.
  7. Risk Factors: immunodeficiency (HIV).
  8. auerus is the most common cause of pyomyositis; it causes up to 75 – 90% of cases.
  9. Pyomyositis presents with fever and pain and cramping localized to a single muscle group. It develops most often in the lower extremity (sites include the thigh, calf and gluteal muscles) but any group of muscles can be involved including iliopsoas, pelvic, trunk, Paraspinal and upper extremities.
  10. MRI is the most useful imaging modality for diagnosing the disease. It can distinguish the defining sites of infection and rule out other entities.
  11. Nonspecific lab findings include Leukocytosis and elevated inflammatory markers but CPK are often normal.
  12. Empiric antibiotics should be directed against Staph/Strep for immunocompetent. Immunocompromised should be covered for Gram negative, gram positive and anaerobic organisms should be considered.
  13. Pyomyositis is graded based on stages.
    • Stage 1 (Invasive stage, 1-2 weeks, may only have pain) can be treated with Antibiotics alone.
    • Most patients present with Stage 2 (Suppurative stage, weeks 3-4)
    • Stage 3 (Late stage) due to delay in diagnosis and usually requires drainage for definitive management.

Case presented by Dr. Michael Hong

Case of the week COW #11

Posted on by Yenis Paez-Perez

CC: Can’t see for 2 months

HPI: 10 year old male with no significant past medical history presents to the Emergency Dept. complaining of painless vision loss in the right eye for 2-3 months. Patient states he has been having difficulty seeing out of his right eye for 2 months despite changing positions in class, taking on and off his glasses and using eye drops. Vision loss has become progressively worse and now he can only distinguish whether lights are on or off. Mother states she did not do anything about this problem because she thought he was kidding and she didn’t’ have money or health insurance to seek medical attention. Patient has been wearing Bifocals for myopia since the age of 6, with corrective vision lenses at age 5. Denies associated trauma. Patient moved to the U.S from Nigeria 5 years ago. He lives with his mother and sister. Vaccines are up to date.

PMH/Birth History: NSVD at 39 weeks, 1 day. Birth took place in Nigeria and mother denies any infection during or after pregnancy. Following birth, patient did not have any complications such as pneumonia, eye infections or rashes.

Social History: Denies drug abuse. Denies exposure to chemicals. Denies contact with dirt, dogs or pigs. Patient did not live on a farm. As per mother, there was no domestic abuse in the family

PHYSICAL EXAM 

Vitals within normal Limits

General: In no acute distress, appears stated age.

Head: Atraumatic, normocephalic. No deformities.

Eye: Right (OD): pupil non-reactive and remains white in color and approximately 2mm. Afferent reflex is present CN II; efferent reflex is absent. There is a complete visual field defect on the right side. Visual Acuity: Can only distinguish between light and dark. Unable to count fingers at any distance or visual objects even in motion. On Fundoscopic exam, the fundus is gray/dull, with no retina visualized. ALL CONSISTENT WITH LEUKOCORIA

Respiratory: Lungs CTA bilaterally.

Cardiac: +S1/S2, no MRG, regular rate and rhythm

Abdomen: soft NT ND

Neuro exam: CN III –XII intact. No motor, sensory, vibratory, temperature or pain deficits. Gait is steady and normal, without any difficulty. Cerebellar function intact, no dysmetria bilaterally.

Extremities: Full ROM in all extremities. 5/5 strength in all extremities

Skin: No edema, rashes, lacerations, or abrasions. Skin is warm, pink, moist and intact.

LABS

CBC: Unremarkable with        WBC: 7.1     Hemoglobin: 13.5       Platelets 211.

CMP: WNL       CRP and ESR = WNL

Tonometry: IOP approx. 17-18 x 3 times

Wood lamp: No corneal abrasion, dendritic ulcers, lesions or depositions OU

Bedside U/S: Completed within 10 minutes of arrival ( Only Right eye is shown)

Working Differential Diagnosis:

  • Retinoblastoma
  • Intraocular Mass
  • Cataract
  • Syphilis
  • Parasitic infiltrate
  • Posterior Infarct

CT Max/Facial w/o Contrast to rule out intracranial pathologies: Negative for masses; positive for homologous material in the right lobe. MRI was recommended for further evaluation

ED/Hospital course:  Ophthalmologist on call was consulted, and said there was nothing more to do. Unfortunately because his vision loss was > 2 months, no life saving surgery was imminent as the retina was already detached causing ischemia to the rods and cones within it.  Patient was to follow up in ophthalmology clinic the following day. Patient’s Pediatrician was also contacted and he referred the patient to a Pediatric Ophthalmic specialist in University Hospital, with a scheduled appointment within the same week. Approximately one week ago, patient underwent surgery and the leading diagnosis was Toxocariasis as per MRI. Biopsy results to follow. As per mother, the patient is still without vision in his right eye.

LEUKOCORIA, UNILATERAL, 10 YO MALE DIFFERENTIALS

Coats disease— is an exudative retinal vascular disorder characterized by retinal telangiectasias and subretinal exudation leading to serous retinal detachment. Presenting complaints include decreased visual acuity, strabismus, or leukocoria. The leukocoria in Coats disease is generally more yellow than white due to the presence of subretinal lipid. Coats disease is almost always unilateral and the vast majority of cases occur in boys. The majority of cases presenting with leukocoria are diagnosed between five and nine years of age, which is older than the majority of retinoblastoma patients.

Clinical examination: subretinal lipid and abnormal telangiectatic vessels US: demonstrates complete retinal detachment with massive subretinal lipid. Intraocular calcification is almost never present in Coats disease, another feature that helps to distinguish it from retinoblastoma.

The retinal photograph depicts bullous retinal detachment in the Left eye of a 1-year-old child with Coat’s disease simulating retinoblastoma. The magnetic resonance images confirm the diagnosis of retinal detachment and exclude retinoblastoma because of the absence of intraocular mass.

 

Toxocariasis — Toxocariasis, or visceral larva migrans, is an infection caused by the dog ascarid Toxocara canis or, less commonly, the cat ascarid Toxocara catis. There may be a history of living in an underdeveloped country, and exposure to dirt or undomesticated dogs. It occurs most commonly in children one to five years of age. Common presenting signs of toxocariasis are strabismus and poor vision. The ocular lesion is caused by the inflammatory response to the second-stage larva, which may localize in the one eye or both eyes

Chorioretinitis characteristic of toxoplasmosis. A pigmented scar is seen with an adjacent area of active chorioretinitis. The diagnosis of toxoplasmosis is based primarily on the appearance of the chorioretinal lesion rather than serologic studies. Courtesy of James T Rosenbaum, MD.

 Retinopathy of prematurity (ROP) — developmental vascular proliferative disorder that occurs in the incompletely vascularized retina of preterm infants and can lead to retinal detachment and permanent blindness. The most important risk factor for developing ROP is prematurity. There needs to be a history of prematurity, and/or mother mentions patient was on O2 for awhile.

Vitreous hemorrhage — Vitreous hemorrhage causes leukocoria when there is extensive organization of the blood into a clot before degradation. With time, the reddish hue of the blood is lost and the hemorrhage transforms into “whitish debris.” Etiology includes advanced ROP,  trauma (MOST common), leukemia or hemorrhagic disease of newborn

Retinablastoma– Retinoblastoma is the most common primary intraocular malignancy of childhood and accounts for 10 to 15 percent of cancers that occur within the first year of life. Retinoblastoma typically presents as leukocoria in a child under the age of two years. Untreated retinoblastoma is a deadly disease; however, with advances in treatment, survival in the contemporary era is >95 percent. Most common age group is birth- 2 years. Very uncommon in children over the age of 5, although 1-2 case reports have occurred in 18 year old males

 Pearls & Takeaways:

  • Leukocoria Requires further investigation – On exam, History and Diagnostic
  • The use of tonometry, fundoscopy and ocular ultrasound are an easy, noninvasive way to add to your ophthalmic exam. Slit-lamp exam could have been considered here
  • Ocular ultrasound is really cool and fun!
  • Advocate for your patients!  Make sure they have proper follow up with a specialist
  • If any abuse or neglect is suspected, be sure to turn on “Sherlock Holmes” senses and investigate.

 

Case presented by Dr. Sarah Bolan

 

Case of the week COW #10

Posted on by Yenis Paez-Perez

CC: Nausea and vomiting and “ I think my sugar is low”

HPI: 36-year-old Female with PMH of Diabetes presents to the Emergency Department complaining of multiple episodes of non-bloody, non-bilious vomiting for the past 5 days. Associated symptoms include chills and a mild sore throat. Denies fever, HA, neck pain, chest pain, SOB, abdominal pain, diarrhea or bloody stools. Denies dysuria, hematuria or urinary frequency or urgency. Denies recent travels or sick contacts.   LMP: Currently menstruating

PMH: Diabetes

PSH: C-Section

Meds: None

Allergies: NKDA

Social: Admits to smoking 2 cigarettes per day for the past 10 years. Smokes marijuana daily. Denies alcohol use

 

Physical Exam : 

BP 171/82   HR 82    RR 20     SpO2 100% on RA    Temp 97.8F     108.86 kg

Constitutional: Alert, wake, and in no acute distress. Obese

HEENT: NCAT, pupils PERRLA, neck is supple. Oral mucosa is pink, dry and intact. No lesions. Normal conjuctiva

Respiratory: CTA B/L, no rales, rhonchi, no stridor or wheezing

Cardiac: +S1/S2, regular rate and rhythm, no murmur, rubs or gallop

Abdomen: Soft, with mild tenderness in epigastric area. No rebound or guarding. Normal BS

Neuro: AAO x 3. No focal deficits, moving all four extremities. Steady gate without difficulty.

MSK/Extremities: no edema, tenderness or swelling.

Skin: Moderate ecchymosis overlying RUQ and RUE. Normal moisture. No rash or lesions noted

 

Pertinent Labs:

WBC: 8.4   HGB: 9.3   HCT: 26.8   Platelet: 9L

Na: 136        K: 3.4          Cl: 104        Co2: 26      BUN: 16     Cr: 0.95   Glucose: 109

PT: 14.4   PTT: 28.7     INR: 1.1

Calcium 8.8         Total Bilirubin: 2.8       Alk Phos: 56           AST: 21                 ALT: 12

Lipase: 60

UCG: negative

Urinalysis: Large Blood with negative Nitrites and Leukocyte Esterase without ketones. UA Protein: 100

 Pertinent Images and other tests: Chest X ray: Borderline heart size. NO active disease

Upper Abdominal U/S: Normal Liver and spleen. The spleen measured 10.9 cm in greatest dimension and was homogeneous in echotexture. No focal splenic lesion identified. The liver measured 16.5 cm and appeared normal.

EKG:

 

Working Diagnosis:

Thrombotic Thrombocytopenia Purpura (TTP)

Idiopathic Thrombocytopenic Purpura (ITP)

Hemolytic Uremic Syndrome (HUS)

Anemia due to blood loss

Infection/Sepsis

ED Course: On further questioning, patient states she has been menstruating for 3 weeks now and bleeding is heavier as compared to the previous cycle. In the ED, patient was given NS 0.9% 1000mL IV bolus once, Zofran 4 mg IV once, Reglan 10mg IV once. Type and screen and blood cultures were also sent and patient was admitted to the Medical ICU for thrombocytopenia and anemia.

Hospital Course:

In the Medical ICU, further lab results demonstrated elevated the following:

LDH: 699         Fibrinogen: 410     Haptoglobin: < 10              Troponin 0.44

Blood Cultures: No Growth

Urine Toxicology: Positive for cannabinoids

Hepatitis C antibody: < 0.1

HIV Ag/Ab: Non reactive

In the ICU, patient was given a 125mg bolus of IV Solu-Medrol and then started on 60mg IV every 8 hours. She was transfused 1 Unit of platelet with no response, as the following day, platelets actually dropped to 5.Hematology/Oncology was also consulted. They stated that the occasional schistocytes seen on blood smear with low Haptoglobin levels and elevated reticulocyte count and LDH was suggestive of microangiopathic hemolytic anemia, making TTP a more likely diagnosis. Heme/Onc recommended against any further platelet transfusion and ADAMS 13 levels were sent. On hospital day #3, patient’s LDH levels had increased to 1586 and Troponin was elevated to 1.2 with symptoms of dyspnea. Patient also had worsening anemia as hemoglobin dropped to 7.0, and platelets remained at 9. The same day, Surgery was consulted and patient was transfused 2 Units of PRBs and 2 Units of FFP in preparation for Shiley Catheter insertion for plasmapheresis. Cardiology was also consulted for the elevated troponin, which they attributed to ongoing demand ischemia without any evidence of ACS. Unfortunately, the following night at 1:25 AM and before a Shiley was ever placed, the patient became minimally responsive and Saturating at 90% on RA. Immediately, she became bradycardic and lost pulses. CPR was initiated as patient was simultaneously intubated. Total duration of CPR was 60 minutes. The patient received Epinephrine x 20, Amiodarone 300 mg x 1 and Insulin with 1 amp of D50W, Calcium chloride and Sodium Bicarbonate for Potassium of 6.1 on ABG. Sadly, the patient was pronounced at 2:25AM.

PEARLS : Thrombotic Thrombocytopenic Purpura (TTP)

PENTAD = ‘FAT RN”

  1. Fever (50%)
    • Uncommon if they present early in the disease
    • High fever and chills suggest sepsis, so look for a source of infection.
  2. Thrombocytopenia
    • MAJOR diagnostic criterion
    • Mean platelet of 25, 000 but they reach 5000.
  3. Microangiopathic Hemolytic Anemia
    • MAJOR diagnostic criterion
    • Non-immune hemolysis with schistocytes
    • Results in elevated LDH, Low haptoglobin and high indirect bilirubin
    • Severely elevated LDH has been associated with MI, arrhythmias, shock and heart failure.
  4. Renal Failure
    • Due to renal thrombotic microangiopathy
    • Urinalysis will show mild proteinuria +/- hematuria
    • Acute Rena insufficiency may be present and may require dialysis.
  5. Neurological Symptoms: (Seizure, AMS, HA, coma, hemiplegia, aphasia, etc.)
    • Focal Deficits less prevalent
    • Occurs in 25-60% of patients
    • Symptoms are usually transient and subtle, so you must ask the patient about prior symptoms!

*** KEEP in mind; all features of the PENTAD do NOT to be present at the same time for diagnosis to be made.

Risk Factors

  • Obesity
  • African American race
  • Female
  • Ages 30-50 years
  • HIV/AIDS
  • Rheumatologic/autoimmune disease history

 Clinical Presentation

  • Fatigue, tachycardia, pallor, SOB or chest pain
  • Abdominal pain, back pain, Nausea, vomiting or diarrhea
  • New Onset jaundice and dark colored urine

Physical Exam

  • Diffuse, non-palpable petechial/purpuric rash.

Etiology

  • ADAMTS-13 protease enzyme deficiency
    • 60% of cases
    • Enzyme cleaves von Willebrand factor (vWF) multimers. Without it, excessive platelet aggregation, thrombocytopenia and thrombosis occurs
  • Idiopathic or Secondary Causes
    • 40% of cases
    • (i.e. HIV, malignancy, Infection, Pregnancy, pancreatitis, autoimmune disease, pancreatitis and medications such s Acyclovir, Quinine, Oxymorphoine, Plavix and Tacrolimus)
  • Diagnosis/Lab findings
    • NORMAL PT, PTT and Fibrinogen levels (Unlike in DIC)
    • Thrombocytopenia
    • Anemia and elevated indirect bilirubin
    • A peripheral smear is important for diagnosis, as 100% of patients will have schistocytes present during the course of the disease
    • ADAMTS-13 activity < 10% (normal activity is > 50%)

*** Remember that TTP is a clinical diagnosis. Do NOT delay treatment!

  • Differential Diagnosis
    • Other Causes of Microangiopathic Hemolytic Anemia (MAHA)
      • DIC, HUS, HELLP Syndrome, Malignant Hypertension, Heparin induced thrombocytopenia, Paroxysmal Nocturnal Hemoglobinuria, etc.
    • ITP
    • Sepsis
    • SLE
    • Viral infections (HIV, mumps, varicella, EBVS)
  • Management
    • Consult Hematology!
    • AVOID Platelet Transfusion if possible!
      • It can lead to renal failure, higher rates of arterial thrombosis and death
      • Should be AVOIDED EXCEPT in life-threatening bleeding or ICH
    • Plasma Exchange (Plasmapheresis) is First Line treatment!
      • Replaces defective or insufficient ADAMTS-13 and clears vWF multimers
      • LDH can be used to evaluate for treatment response
    • FFP Transfusion
      • Contains ADAMTS-13
      • Can be helpful if delay in plasmapheresis
    • Transfusion of RBCs (indicated ONLY in severe bleeding with a delay in plasma exchange)
    • Glucocorticoids
      • Adjunct Treatment and do not replace plasmapheresis
      • 1mg/kg Prednisone PO or Solu-Medrol 125mg IV
    • IVIG
      • Not first line but may be used in those who fail plasmapheresis
    •  Splenectomy
      • Last line therapy after stabilization
      • Inhibitor antibody is made in the spleen

Suspect TTP in any patient with MAHA and thrombocytopenia!

Case presented by Dr. Yenisleidy Paez Perez, DO

Case of the Week COW #9

Posted on by Yenis Paez-Perez

CC: “Post Surgical Pain” ; Abdominal pain

HPI: 8 year old Male with PMH of Sickle Cell Disease (HbSC), Post-opt Day 10 for laparoscopic splenectomy for recurrent sequestration crises presents to the Emergency Department (ED) complaining of abdominal pain x 2 days. The pain is described as diffuse and worse in the RUQ. Denies exacerbating or relieving factors. Pain is associated with constipation; last Bowel movement was 7 days prior. Mother states he did have one small BM shortly after surgery. He is tolerating PO without difficulty and does report flatus. She has been giving him Oxycodone 2mg every 6 hours for pain with minimal relief. Upon review of systems, patient reports feeling hot for the past 2 days but without a recorded temperature at home. Additionally, patient complained of a non-productive cough for 2 days and has been “breathing fast” for the same duration of time.

Physical Exam:

BP 112/74    HR 129     RR 24   SpO2 93% on RA   Temp 99.9F      26.3 kg

Constitutional: Well developed, well-nourished child who is awake, alert and in moderate distress due to pain and feeling hot; making tears

HEENT: NCAT, pupils PERRLA, neck supple

Respiratory: CTA B/L, no wheezing, rales or rhonchi

Chest/Axilla: Normal symmetrical motion, no tenderness

Cardiac: +S1/S2, RRR, no MRG,

Abdomen: Scars noted over splenectomy site which are clean dry and intact, healing well without discharge; Diminished Bowel Sounds in all quadrants; soft, non-distended with mild tenderness in all 4 quadrants. No rebound or guarding.

Neuro exam: AAO x 3. No deficits

Extremities: no edema, no tenderness or swelling

Pertinent Labs:

CBC: 42.1

HBG: 12.5

HCT: 36.9

Platelets: 721

Seg: 79

Lymphs: 9

Mono: 12

Reticulocyte count: reported as normal

Pertinent Imaging and other tests:

Working Diagnosis:

Generalized abdominal pains

Elevated WBC

Abscess of spleen

ED/Hospital course:

Surgery was consulted in the ED and they believed the pain was not related to the surgery. Abdominal U/S performed at their request showed “s/p splenectomy with gallbladder sludge.” Patient had moderate improvement in his pain after Toradol 15mg IV and Morphine 2mg IV were given in the ED. Patient also received Rocephin 75mg/kg and NS 500mL IV Fluid bolus for presumed infection with the leukocytosis of 42.1.

The patient was admitted to Pediatric Step down for further evaluation and management. Overnight, he remained comfortable with stable vital signs, afebrile and saturating 94-96% on 2L NC. On Hospital day #1, patient became febrile to 103F and continued to deny chest pain, SOB or difficulty breathing. The cough remained unchanged since admission. A repeat Chest X-Ray was obtained and the patient was diagnosed with Acute Chest Syndrome and received exchange transfusion the same day (Refer to Image below) Additionally, he received Ceftriaxone, Azithromycin, Nitric oxide and IVF at ¾ maintenance ate throughout hospitalization. On Hospital Day #4 he was discharged home.

Pearls:

Acute Chest Syndrome

  • It is the leading cause of death in patients with SCD in the United States
  • Most often occurs as a single episode, but patients may have multiple attacks resulting in chronic lung disease
  • Multiple Etiologies
    • Pulmonary infections
    • Iatrogenic cause including aggressive hydration for sickle cell painful crisis ——à causing Pulmonary Edema
    • Opioid use —–à Decreased inspiratory effort——à Atelectasis
  • New infiltrate identified on Chest X-Ray with at least one of the following: Fever, cough, wheezing, tachypnea, chest pain, hypoxemia.
  • Radiographic changes often lag behind clinical features so initially the Chest X-Ray may actually be normal (as in our case)
  • Treatment
    • Supportive: Early Supplemental Oxygen, analgesics and IV Hydration up to 1.5x maintenance rate
    • Antibiotic irrespective of cultures
    • Transfusion is believed to be lifesaving; recommendations based on empirical observations and not on firm evidence
    • Exchange transfusion seems to be more advantageous, especially in patients with a hemoglobin of > 9.0
      • It decreases the concentration of sickled hemoglobin with little iron gain
    • Inhaled Nitrous Oxide is beneficial
      • Due to its vasodilatory effects –à improved ventilation/perfusion in damaged lung tissue
      • Reduced RBC and leukocyte adhesion to endothelial cells, therefore affecting disease progression
    • Hydroxyurea reduces occurrence of acute chest syndrome

Case Presented by Greg Cassidy, MD

 

References:

  1. Stapczynski, J. S., & Tintinalli, J. E. (2016). Tintinalli’s emergency medicine: A comprehensive study guide (8th ed.). New York, N.Y.: McGraw-Hill Education LLC..