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Euglycemic DKA

Hi all. I wanted to bring to your attention a great case. The case was a young woman with relative euglycemic diabetic ketoacidosis. This diagnosis used to be quite rare and associated with pregnancy or very poor PO intake. However, with the use of SGLT2 inhibitors (which this young woman was taking) the incidence is increasing. The diagnosis highlights some very important factors about the treatment of DKA:

  • Don’t just look at the blood sugar. Calculate your anion gap. Look at the bicarb. Calculate the strong ion difference. Check for ketones. A VBG is fine for a rough estimate of pH. If you really want to get fancy, an ABG will give you an accurate base deficit that can help you figure out (along with your lactic acid, strong ion gap, or delta-delta) exactly what else is going on with the patient in the setting of multiple competing metabolic processes. But that’s only if you want to get fancy. I think you can provide great initial resuscitation without it.
  • Remember why we do what we do in DKA and all the complications you can get from treatment. The treatment is based on exactly the same principles that guide the treatment of “regular” DKA. However, they are not starting at the exact same metabolically disturbed place as most patients do. They can be just as sick, if not more, but the initial treatment has to take into consideration exactly where they are in their metabolic disarray. Things to think about as you are coming up with a treatment plan:
  • These patients need fluid. Fluid will be your friend (more on that later)
  • These patients need glucose. From the start. For a glucose less than 100-125, consider starting D10 instead of D5.
  • They need glucose because they need insulin too. They still may have some relative insulin resistance so giving them glucose alone won’t help them if they cannot get the glucose into any cells. However, as you are already starting from a lower glucose, be very gentle. If you still bolus insulin in DKA (which I do- in selected cases- and would be glad to have conversation about whether we should or not at another time) do NOT bolus these patients. I don’t have great evidence as to where to start a drip so I pick a low number. Like 1 low. I can always move up. If anyone has a better scientific explanation on how to pick your infusion rate, I’d love to hear it.
  • They need insulin so you better be sure you aren’t going to cause a malignant arrhythmia if you give it to them. Make sure your potassium isn’t going to plummet when you start insulin. Rough guideline is to make sure it is >3.3 . This is true for all DKA.
  • They don’t have a sodium correction because the glucose is normal. If their sodium is already on the higher side (around >140), think of starting with ½ NS as your base.

The attending on the case did an excellent job with this patient. He focused on fluid and recognized her severe metabolic disturbance, despite the fact that her blood sugar was trying to hide it.

I’ve included two articles below. One is two case reports on euglycemic DKA and the other talks specifically about cases involving SGLT2 inhibitors. They aren’t the best articles I’ve ever read but they are more official than I am so felt I should include them. As a said, this is a relatively new class of medications and a relatively new phenomenon.


Euglycemic diabetic ketoacidosis: a diagnostic and therapeutic dilemma, EDM Case Reports, September 2017

Posted by:

Ruth Lamm, MD FACEP
Assistant Professor
Emergency Medicine
Critical Care Medicine
Saint Joseph’s Hospital Medical Center
lammr@sjhmc.org

Case of the week COW #10

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

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..

 

EM Conference Pearls (9/20)

Pediatric congenital heart disease

  • Congenital HD: Two types: Neonates with ductal dependent lesions and infants (2-6months) presents with CHF
  • Cyanosis presentation: When ductal-dependent lesion is required for pulmonary blood flow (Will not respond to oxygen)
  • Shock presentation: When ductal-dependent lesion is required for systemic blood flow (appear septic and not response to fluids, may get worse with fluids)
  • Hypoxic/cyanotic or shocky/acidotic baby treatment = Prostaglandin E1 (PGE1) and transfer to facility with pediatric cardiovascular surgeon.
  • PGE1 treatment may cause apnea (monitor closely and consider intubation)
  • CHF in infants = wheezing, retractions, tachypnea, sweating/crying, difficulty feeding

EBM in the ED

  • EBM = What the evidence shows in the literature + What the physician wants for the patient + what the patient wants for themselves
  • Just like we need to practice intubation, central lines –> Learning to read and interpret literature is a skill that needs to be practiced.

Aortic Dissection

  • AD: Chest pain plus disease (ex: CP + Neurodeficit)
  • If you find your self giving large amounts of strong pain meds (narcotics) while treating what is seemingly ACS…STOP..think about AD or alternative diagnosis of chest pain
  • The 3 important questions, aortic dissection is the subarachnoid hemorrhage of the torso, migrating pain, colicky pain + opioids = badness and pain that comes and goes can still be a dissection.
  • Treatment: Treat pain, HR, BP
  • Pain: Fentanyl 25 – 50 mcg bolus
  • HR: Goal of 60 bbpm
  • Esmolol 0.5 mg/kg bolus then 50 – 300 mcg/kg/min or
  • Labetalol 10 – 20 mg bolus then 0.5-2 mg/minor
  • BP control: Goal SBP =110
  • Nitroprusside 0.25 – 0.5 mcg/kg/min then titrate (CN toxicity)
  • Nicardipine 5 mg/hr
  • Warning: Giving a vasodilator without concomitant reduction in ionotropy may cause progression of dissection. Start BB first before vasodilation meds.

Case of the Week COW #8

CC: Altered Mental Status

HPI: 50 -year-old Male with PMH of HIV, CVA and Meningitis presents to the Emergency Department (ED) for altered mental status. As per the patient’s girlfriend at bedside, the patient woke up confused and was not making any sense when he spoke. He even urinated on the floor but does not remember doing so. Patient had been complaining of back pain, testicular pain and leg pain for the past couple of weeks and had been evaluated for it in the ED. Patient also states he is currently taking “something for his HIV” but is unclear what his last CD4+ count was. Denies sick contacts. The rest of the review of systems was limited by confusion, but denied vomiting, diarrhea, abdominal pain, or any other complaints.

Physical Exam:

BP 128/78   HR 129     RR 14   SpO2 96% on RA   Temp 102.4F

Constitutional: Diaphoretic, confused and intermittently following commands.

HEENT: NCAT, pupils PERRLA, neck supple

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

Cardiac: +S1/S2, tachycardia, no MRG, regular rhythm

Abdomen: soft, mildly distended with mild tenderness in RUQ and LUQ.  Was not able to appreciate any focal masses . No rebound or guarding

Neuro exam: Not oriented to time or situation, No focal deficits, moving all four extremities. Unable to complete a more detailed exam as patient remained confused.

Extremities: no edema, no tenderness or swelling

Skin: pink and warm with diaphoresis, no rashes, lacerations, or abrasions

Pertinent Labs:

(Per Sorian Inpatient) CD4 = 120 on June 2017

Sepsis workup summary (normal if not reported):

  • Trop 0.045ng/ml
  • Sodium 126
  • WBC 5.8       Chloride 93
  • RBC 3.72      CO2 19
  • HBG 10.3      Glucose 116
  • HCT 30.3       BUN 89
  • Platelets 108
  • Cr 2.90 (↑ from baseline)
  • Bands 27        Total Bili 4.5
  • Lymphs 3       Total Protein 5.7
  • Monos 2         Albumin 2.6
  • Lymphocytes 0.2
  • Alk Phos 346   Monocytes 0.1
  • AST 143
  • ALT 58
  • Lactic acid 3.4
  • U/A negative
  • CSF negative

Pertinent Imaging and other tests:

EKG remarkable for sinus tachycardia, left axis deviation, and an old RBBB

CT head w/o contrast remarkable for only mild frontal volume loss

Chest XR – unremarkable

RUQ Bedside US and then official US completed and showed:

Working Diagnosis:

Hepatic hydatid cysts from Echinococcus tape worm

Hepatic abscesses

Metastatic cancer

Multiple biliary hamartomas

Polycystic liver disease

Caroli Disease

ED/Hospital course:

In the ED, the patient received IV Fluid boluses of NS 30mg/kg and one 1000mL of NS along with Tylenol, Vancomycin and Zosyn. The patient was admitted to Infectious Disease service. Throughout the hospital stay, CT Scan of abdomen and pelvis w/o contrast (due to AKI) was remarkable for infiltrated liver, splenic lesions, and destructive lesions of the bilateral iliac wings and L5 with pathologic fracture of the posterior right rib, which may be due to metastatic disease. The underlying etiology is uncertain. Without contrast, it was not certain if there was underlying macronodular cirrhosis. There was also associated ascites. Initial blood cultures from the ED grew Salmonella species. The patient was initially admitted the medical floor but was transferred to the Medical ICU on day 7 of hospitalization for increased lethargy and worsening lactic acidosis, transaminitis, and AKI. He later went into multisystem organ failure and was intubated thereafter. His code status was also changed to DNR/DNI. The patient unfortunately expired before endoscopy, colonoscopy, and biopsy could be performed.

Official Ultrasound read – Findings consistent with metastatic disease to the liver.

Pearls:

Hepatic Hydatid infection

  • Caused by Echinococcus granulosus or Echinococcus multilocularis
  • granulosus – Endemic in North America & Australia with dogs & wolves main as main host
  • multilocularis – Found in Northern Hemisphere with red fox, dogs, & cats as main host
  • Ultrasound would show a multiseptate cyst with daughter cysts
  • X-ray would show calcified rings
  • CT Abd/Pelvis may show the water-lily sign, which occurs when the endocystic membrane becomes detached, resulting in floating membranes within the pericyst, which mimics the appearance of a water lily ( Refer to Figure 1).

Figure 1. A detached membrane within the contents of the cyst, known as the water-lily sign

Pearls

Hepatic Hydatid infection

  • Infection may be asymptomatic for many years, with a long latent period (up to 50 years of age!)
  • Albendazole for confirmed infection
  • Reserve antibiotics for those in which diagnosis is uncertain due to risk of anaphylaxis
  • Most cases in U.S. occur in immigrants from endemic countries (South America, Middle East, eastern Mediterranean, sub Saharan, African, West China, former Soviet Union)
  • Confirmed cases in U.S. are rare

Patients with HIV

  • Always ask for CD4+ count and if they are on medications for their HIV/AIDs
  • Have a low threshold for doing an aggressive workup for these individuals, especially if poor follow up
  • HIV is a risk factor for Salmonella bacteremia
    • Other risk factors include any immunosuppressed state, liver disease, hemoglobinopathies (decreased splenic function)
    • Most salmonella bacteremia can have a preceding diarrheal illness
    • Major complication is endovascular infection
    • Treatment is IV fluoroquinolones or 3rd generation cephalosporin

Case presented by Jessica Williams, MD, PGY1

Case of the Week COW #7

CC: Numbness and palpitations

HPI: 21-year-old Female presents to the Emergency Department (ED) complaining of palpitations and left arm weakness with perioral numbness, which began just prior to arrival. The patient states the episode lasted 30 minutes before completely resolving on its own. In the ED, she denies any other complaints except for a mild headache. Patient notes she experienced a similar episode of palpitations yesterday afternoon, while resting, which she described as “skipping beats”. On further questioning, the patient admitted to being hospitalized to a NYC hospital 2 weeks ago where she had a Cardiac Echocardiogram done which showed “hypertrophy.” Patient never followed up with cardiologist as instructed. In the past, a doctor in her country prescribed her an unknown antihypertensive medication, which she took for one year but stopped taking it once she moved to NJ. Denies fever, dizziness, chest pain, and shortness of breath, recent travels, calf pain or swelling.

Physical Exam:

BP 109/72   HR 82     RR 18     SpO2 100% on RA    Temp 97.0F

General: Well appearing female, in non-acute distress

HEENT: NCAT, pupils PERRLA, neck supple

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

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

Abdomen: soft NT ND

Neuro exam: AAO X 3, No focal deficits

Extremities: no edema, no tenderness or swelling, 5/5 strength in all extremities. Sensory intact

Skin: pink and warm, No diaphoresis, no rashes, lacerations, or abrasions

Pertinent Labs: Troponin 0.308

Pertinent Imaging and other tests:

  • Chest X-Ray: Cardiomegaly with a boot shaped heart, which may indicated right heart failure.
  • CT Head: Normal 
  •  ECG: Normal Sinus Rhythm, Bi-atrial enlargement, RBBB, LVH

Working Diagnosis: Hypertrophic Cardiomyopathy (HCOM)

ED/Hospital course:  Patient was given 324 mg of ASA and admitted to Telemetry with a diagnosis of Hypertrophic Cardiomyopathy. While still in the ED waiting for a bed on Telemetry the patient had multiple runs of non-sustained V-Tach and Cardiology was consulted. The patient was started on ASA and Metoprolol PO. A 2D ECHO was done which was consistent with HCOM. Patient remained stable on Telemetry for 3 days prior to discharge. The patient’s Troponin was trended daily, 0.308 in the ED, 0.288 on day 1 of admission, and 0.314 on day 2 of admission. Patient was told to follow up with Cardiology Clinic for possible AICD placement planning.

Pearls:

Hypertrophic cardiomyopathy (HCM) is one of the most common inherited cardiac disorders (affecting ~ 1 in 500 people) and is the number one cause of sudden cardiac death in young athletes. Annual mortality is estimated at 1-2 %.

  • Pathology and Pathophysiology:
    • Dynamic Obstruction of the Left Ventricular Outflow Obstruction (LVOT)
    • Primarily Autosomal Dominant Inheritance
    • Left Ventricular diastolic dysfunction resulting from impaired relaxation and filling of the stiff and hypertrophied left ventricle (often associated with increased filling pressure)
    • Abnormal intramural coronary arteries with thickened walls and narrow lumens
    • Chaotic, disorganized left ventricular architecture (“ cellular disarray’) predisposing to abnormal transmission of electrical impulses and thus serving as a substrate for the formation of arrhythmia.
  • Clinical Manifestation
    • Exertional syncope or pre-syncope – this is the most worrisome symptom, suggesting dynamic LVOT obstruction with or without dysrhythmia, with the potential for sudden cardiac death.
    • Symptoms of pulmonary congestions due to left ventricular dysfunction (e.g. exertional dyspnea, fatigue, orthopnea, paroxysmal nocturnal dyspnea)
    • Chest pain – may be typical angina pain due to increased demand (thicker myocardial walls) and reduced supply (aberrant coronary arteries).
    • Palpitations due to supraventricular or ventricular arrhythmias.
  • ECG Features:
    • Left atrial enlargement
    • Left ventricular hypertrophy with associated ST segment / T-wave abnormalities
    • Deep, narrow (“dagger-like”) Q waves in the Lateral (V5-6, I, aVL) and inferior (II, III, aVF) leads. Most common in Lateral vs. Inferior
    • Giant precordial T-wave inversions in apical HCM
    • Signs of WPW (Short PR, delta wave)
    • Dysrhythmias: Atrial Fibrillation, supraventricular tachycardia, PACs, PVCs, VT

*** Infarction Q Waves are wider with a different morphology compared to HCM.

Pathologic Q Waves:

  • Usually > 40 ms (1mm) wide
  • > 2mm Deep
  • > 25% of depth of QRS Complex
  • Best seen in V1-V3

 

Post by Tyler Manis, MD, PGY4

ACEP Now Review on LVADs

Check out this excellent review on managing patients with LVADs from this month’s ACEP Now publication which was written by our own Dr. Yenisleidy Paez Perez, DO PGY-3 and one of our newly graduated residents, Dr. Terrance McGovern, DO. The article is entitled ‘How to Manage Emergency Department Patients with Left Ventricular Assist Devices.” Click the link below to be forwarded to the article.

http://www.acepnow.com/article/manage-emergency-department-patients-left-ventricular-assist-devices/

Breaking Bad News

One of the hardest roles of the emergency physician is giving bad news to a patient or their family members. Difficult topics that are often challenging for physicians to discuss include reporting the death of a family member or giving the diagnosis of a terminal illness. The optimal way to relay these topics is yet to be determined and each practitioner typically develops their own communication style. Some choose to deliver the message in a direct and succinct manner while others prefer a more drawn out and complete explanation. The Emergency Department provides a unique environment as there is often little time to develop any rapport with the patient and their family. This can make communicating these topics more challenging. In addition, breaking bad news involves more than just the verbal component of actually giving the bad news. It also requires the ability to respond effectively to patient’s and family’s emotional reactions and the dilemma of how to give hope when the situation is bleak.

Jurkovich et al studied the characteristics and methods of delivering bad news from the perspective of surviving family members. The chart below details the importance of various elements rated by respondents in the study. The attitude and clarity of the message delivered by the provider were deemed to be most important, while the attire of the provider had little importance to the respondents.

The duty of breaking bad news can be improved by understanding these characteristics and methods and then applying a step-wise method to effectively communicate and counsel patient’s and/or their families. In a recent Wednesday conference, Dr. Flannery, one of our core faculty attendings, introduced us to the SPIKES protocol for breaking bad news. The purpose of the protocol is to help the clinician fulfill the essential goals of gathering information, providing intelligible information, and supporting the patient or family by reducing their emotional impact and isolation. When we are informing our patients of an unfortunate diagnosis, the protocol also calls for collaborating in developing a strategy or treatment plan for the future. From the Emergency Department standpoint, this means guiding patients to the correct consultant for further workup and treatment options.

During our Wednesday conference, we broke into small groups and practiced situations that would be considered difficult to give bad news. The experience was positive and allowed us to give each other constructive criticism on ways to improve our approach to giving bad news. As a senior resident, I have unfortunately been involved in many of these situations throughout my residency. I have learned that despite the challenges involved in delivering bad news, there is also tremendous gratification in providing a therapeutic presence during a patient or family’s greatest need.

References:
1. Jurkovich et al. Giving bad news: the family perspective. J Trauma. May 2000
2. Baile W.F. et al. SPIKES – A Six-Step Protocol for Delivering Bad News: Application to the Patient with Cancer. The Oncologist. June 12, 2000.

EM Conference Pearls (8/2/17)

Pearl’s from Wed conference August 2nd 2017:

Agenda:
– Asthma/COPD: Baldino
– Sepsis Core Measures: Patel
– Pulmonary cases: Patel
– Medical student pearls (from Mike Taylor, one of our students)


Dr. Baldino: Asthma/COPD

-All that wheezes is not asthma (or COPD).
-Use diagnostics to rule out mimics such as pneumonia or ptx.
-Get the CXR in COPD exacerbation, not routinely in simple asthma exacerbation.
-Good evidence and NNT’s for benefit of ipratropium, systemic steroids, magnesium,  and BiPAP.
-Intubation last resort for asthma.  Remember to adjust I to E ratio on vent.
-Steroids at discharge for asthma/COPD.  Antibiotics at discharge for COPD.
-Discharge with a plan! (and a spacer)


Dr. Patel: Sepsis Core Measures

-Sepsis core measures are from CMS, not from SSC guidelines or Sepsis 3.0. They are not necessarily rooted in great evidence, but we have to follow them!
-Remember the 3 and 6 hour severe sepsis and septic shock bundles. Timing is based on presentation time (when chart displays severe sepsis, septic shock), not door time.  To make your life easy, just use door time to meet the metrics.
-The focused exam for septic shock can now just be documented with one statement, which is in Medhost.  Make sure to click that.
-Fluids from the field count (as your 30 cc/kg), as long as it is given as a bolus and documented on the chart.
-Antibiotic choice and timing both looked at for core measures. For choice, best to go with a monotherapy agent first to meet the metric.


Dr. Patel: Pulmonary Cases

-The term HCAP is not in the newest pneumonia guidelines from 2016.
-Treat HCAP like CAP unless the patient is going to the MICU.  If going to the MICU, cover for MRSA and Pseudomonas.

Hemoptysis:

-Minor hemoptysis (streaks in the sputum)–d/c unless CXR abnormal
-Moderate hemoptysis (frank hemoptysis)—admit for further work up and obs
-Massive hemoptysis (hemoptysis interfering with respirations)–intubate and consult pulmonary (for bronch) and IR (for possible bronchial artery embolization). If there is a suspicion of a bronchovesicular fistula or other arterial fistula, CT surgery may also need to be on board.


Medical Student Pearls

One of our current medical student’s Mike Taylor put together some info on questions that were raised in conference:

Intentional “L Main Bronchus Intubation:” (for hemoptysis)

Take Home Points from 1995 Anesthesiology Case Report:
 -Can use a double lumen ET tube with a endobronchial cuff
 -The inflated endobronchial cuff can tamponade the hemorrhaging R lung and occlude airflow into it. This allows only the L lung to be effectively intubated and the provider not have to be tasked with putting the tube in the L main bronchus
 Reference: http://anesthesiology.pubs.asahq.org/article.aspx?articleid=1949905

Rate Control for MAT:

Take home points from Uptodate
 -Treat underlying cause
 -Maintain phos and mag levels
 -Can use CCBs or beta blockers for rate control in symptomatic pts
 Reference (requires access to UpToDate): https://www.uptodate.com/contents/multifocal-atrial-tachycardia

Bandemia Cut Offs:

Take home points from 2012 Retrospective Cohort Study:
 -With normal white counts, pts with bandemia of at least 11% had higher in hospital mortality
 -So 11% or higher could use as a cut off for admission, more aggressive treatment, etc.
 Reference: https://www.ncbi.nlm.nih.gov/pubmed/22939096

Special thanks to Chief Dan Poor PGY-4 for organizing this week’s Conference Pearls and for Mike Taylor MS-IV for his Medical Student Pearls

Case of the week COW #6

CC: Vomiting for 2 days

HPI: 32 yo female with PMH of Romano Ward Syndrome s/p AICD, previous cardiac arrest, Atrial Fibrillation s/p Ablation, renal artery thrombosis on Coumadin and deafness presents to the Emegency Department (ED) via ALS after being found unresponsive at home and with ventricular tachycardia. Paramedics state they were called to the patient’s home for an “unconscious” person. They arrived to find the patient lethargic but arousable, cool, pale, and diaphoretic with BP 90/50. The patient soon became unresponsive and was in Ventricular tachycardia on the monitor. Patient underwent synchronized cardioversion with 150 Joules and converted to sinus tachycardia. Patient also received 150 mg Amiodarone bolus and 250 mL of Normal Saline IVF. Patient’s sister arrived to ED approximately 10 minutes after patient’s arrival and states that patient had multiple episodes of becoming unconscious at home earlier today. Denied recent illness, fever/chills, vomiting, diarrhea

Physical Exam:

BP 133/105,   HR 115 Sinus tachycardia,   RR 20,   SpO2 100% on 3 lpm NC,    Temp 97.0F

General: Lethargic but arousable to painful stimuli

HEENT: NCAT, pupils PERRLA, neck supple

Respiratory: Moderate respiratory distress with bibasilar rales, otherwise clear, no wheezing

Chest: AICD in left anterior chest

Cardiac: +S1/S2, no MRG, tachycardia, regular rhythm

Abdomen: soft NT ND

Neuro exam: arousable to painful stimuli, pt reading lips, answering appropriately

Extremities: weak thready pulses throughout, no edema

Skin: cool, pale, diaphoretic, no rashes, lacerations, or abrasions

 Labs:

CBC: Unremarkable     CMP: K 3.2   Glucose 595     BUN/Cr 17/1.62

AST/ALT 359/401       INR: 1.7             Troponin 0.122

ED Course: Approximately 5 minutes after arrival to the ED during the initial exam, patient became unresponsive and was noted to be in Ventricular Fibrillation on the monitor. CPR/ACLS was started and patient was intubated immediately. Her defibrillator appeared to be delivering shocks however there was no conversion of the rhythm. ACLS was performed for 30 minutes and pulses were regained multiple times. Patient was in V-fib, then PEA, then V-tach arrest. 100mg Lidocaine and 2 grams Magnesium were also given. Defibrillation with external pads ultimately led to Return of Spontaneous circulation. Bloody, frothy sputum was also noted from the ETT post-arrest. A right IJ central line was placed

EKG:

Pre-arrest: Atrial-paced with PACs. QTc 503      Post-arrest: Atrial tachycardia. QTc 609

DX: VFib & VTach arrest s/p ROSC in the setting of Congenital Long QT syndrome and AICD non-capture.

ED/Hospital course:  Post-ROSC EKG did not show STEMI. Post-ROSC Chest XR demonstrated diffused pulmonary edema. Patient was hypoxic with SpO2 in the 80s on 100% FiO2. Decreased tidal volume and increased PEEP improved oxygenation. Bedside cardiac Ultrasound showed global hypokinesis and no pericardial effusion. CT Head w/o contrast was normal. Amiodarone drip was started. Hypothermia protocol was initiated. The patient was admitted to the CCU. She did not code again while in the ED. Her AICD was interrogated and it showed she had been in sustained Vtach to which her AICD gave multiple shocks without capture. She was in the hospital for 11 days where she initially was improving and was therefore extubated after 7 days. Unfortunately she again went into Vtach arrest multiple times and then PEA arrest and was pronounced dead.

Pearls:

Congenital Long QT Syndrome (LQTS)

  • The major variant of congenital prolonged QT syndrome (there are 6 total). Affects estimated 1/2500 to 1/7000 people worldwide
  • Can have varying degrees of penetrance
  • Thought to account for ~3000/year of sudden deaths in children
  • May play a roll in prevalence of SIDS
  • Autosomal dominant inheritance, results in mutation of genes responsible for creating ion-channel proteins. The impaired transport of ions in cardiac tissue causes prolonged QT à impaired repolarization à ventricular arrhythmias (symptomatically syncope, seizure, cardiac arrest). May also present with AV blocks and bradydysrhythmias.
  • Romano-Ward is the more common, autosomal dominant (AD) form with purely cardiac phenotype.
  • The Jervell and Lange-Nielsen syndrome refers to the autosomal recessive (AR) phenotype of congenital LQTS that is associated with profound sensorineural hearing loss and a high risk for sudden death. MORE MALIGNANT CLINICAL COURSE. Our patient likely had this variation since she also had deafness.

Management and treatment

  • Beta- blockers = 1st line treatment in symptomatic patients. Blunts catecholaminergic response
  • Whenever syncopal episodes recur despite full-dose beta-blocking therapy, left cardiac sympathetic denervation (LCSD) should be considered. Cardiac pacing is only rarely indicated (e.g. in infants or young children with 2:1 atrioventricular block).
  • Implantable cardioverter defibrillators (ICDs) are always indicated after cardiac arrest, or when requested by the patient, and whenever syncope recurs despite beta-blockade and LCSD.
  • Potassium supplementation or spironolactone
  • Other antiarrhythmic therapy based on genotype

Risk Factors  for syncope or SCD

  • Congenital deafness
  • Hx/o syncope
  • Hx/o Ventricular arrhythmia
  • Family hx/o SCD
  • Female gender
  • QTc > 600ms
  • Medical non-compliance

Event triggers (vary depending on which genetic mutation)

  • Exercise-related
  • Auditory stimuli (alarm clock, telephone ringing!)
  • Acute emotional events
  • Catecholamine-induced
  • Pregnancy and up to 9 months post-partum
  • Onset of menopause

Post by Katrina D’Amore, DO.