Ectopic Pregnancy

HPI:

32F G8P7A2 at 5 weeks by LMP presenting with abdominal pain. The patient reports acute onset of sharp left lower abdominal pain 1.5 hours prior to presentation. The pain has been constant since onset, 10/10 in severity, radiating to lower back and exacerbated with movement. She denies vaginal bleeding or discharge, passage of clots or other products. She also denies trauma, lightheadedness/dizziness/syncope, shortness of breath, nausea/vomiting or changes in bowel or urinary habits.
Her pregnancy was detected 3 weeks ago with a home pregnancy test and was confirmed at her PCP one week later. She has not had an ultrasound during this pregnancy but has a history of uterine fibroids. She has no history of sexually transmitted infections, prior ectopic pregnancy, or use of assisted fertilization.

PMH:

  • HTN
  • Uterine fibroids

PSH:

None

FH:

Non-contributory

SHx:

  • Denies tobacco, alcohol or drug use.
  • Sexually active with husband only, no history of STI.

Meds:

None

Allergies:

NKDA

Physical Exam:

VS: T 37.4 HR 108 RR 36 BP 148/104 O2 99% RA
Gen: Alert and oriented female, appears uncomfortable due to pain.
HEENT: PERRL, EOMI, MMM.
CV: Tachycardia, regular rhythm, no murmurs.
Lungs: CTAB, no crackles.
Abd: Normoactive bowel sounds, tenderness to palpation in LLQ and suprapubic area, with guarding but no rebound tenderness. No CVAT.
GU: No external lesions. Closed cervical os, no blood or discharge, +CMT.
Ext: Warm, well-perfused with strong peripheral pulses.

Labs/Studies:

  • POC Hemoglobin: 11.8
  • POC ICON: positive

Imaging:

Bedside Ultrasound

  1. Transabdominal: Free fluid in hepatorenal and splenorenal recesses
  2. Transvaginal: Free fluid and debris in posterior cul-de-sac, likely pseudogestational sac in endometrial cavity, no IUP identified. Formal ultrasound revealed fetus with cardiac activity in left adnexa.
Hepatorenal free fluid

Hepatorenal free fluid

Free fluid in the hepatorenal recess (Morison's Pouch)

Splenorenal Free Fluid

Splenorenal Free Fluid

Free fluid in the splenorenal recess.

Pelvic Free Fluid

Pelvic Free Fluid

Free fluid and debris in the posterior cul-de-sac.

Pseudogestational Sac

Pseudogestational Sac

No obvious yolk sac or fetal pole.

Assessment/Plan:

32 year-old ICON positive female with acute-onset pelvic pain. The patient remained hemodynamically stable and absence of definitive IUP on bedside ultrasound was confirmed with presence of fetal cardiac activity in left adnexa indicative of ectopic pregnancy. OB-Gyn was consulted and the patient was taken emergently to the OR.

Differential Diagnosis of First Trimester Abdominal Pain: 1

Differential Diagnosis of 1st Trimester Abdominal Pain

Initial Evaluation of First Trimester Abdominal Pain: 1

  • 2 large-bore IV’s, begin fluid resuscitation
  • POC testing: hemoglobin, urine pregnancy
  • CBC, type and cross (Rh), serum B-hCG
  • Emergent bedside ultrasound

Features Associated with Ectopic Pregnancy: 1

  • History
    • PID
    • Tubal ligation
    • Prior ectopic
    • IUD
    • Assisted fertilization
  • Physical
    • CMT
    • Peritoneal irritation
  • Ultrasound
    • Empty uterus
    • Adnexal mass
    • Free fluid
  • Ultrasonographic Findings in the Evaluation of Ectopic Pregnancy: 2

    • Discriminatory hCG (1500-3000 mIU/mL): absence of IUP suggests ectopic or abnormal gestation
    • Normal IUP
      • 4-5wks: gestational sac (0.2-0.5cm)
      • 5wks: two echogenic rings
      • 5.5wks: yolk sac
      • 6wk: embryonic pole
      • 6.5wk: fetal cardiac activity
    • Abnormal IUP
      • >2cm gestational sac without fetal pole
      • CRL >0.5cm without cardiac activity
    • Ectopic
      • Extrauterine gestational sac with or without cardiac activity
      • Extrauterine ring sign
      • Non-homogenous adnexal mass

    Contraindications to Medical Management: 2,3

    • Absolute
      • Breast-feeding
      • Immunodeficiency
      • PUD
      • Pulmonary, hepatic or renal dysfunction
    • Relative
      • Ectopic mass > 3.5cm
      • Fetal cardiac activity

    References:

    1. Dart, R. (2003). First Trimester Emergencies A Practical Approach To Abdominal Pain And Vaginal Bleeding In Early Pregnancy. EB Medicine, 5(11), 1–20.
    2. Barnhart, K. T. (2009). Clinical practice. Ectopic pregnancy. The New England journal of medicine, 361(4), 379–387. doi:10.1056/NEJMcp0810384
    3. Jurkovic, D., & Wilkinson, H. (2011). Diagnosis and management of ectopic pregnancy. BMJ (Clinical research ed.), 342(jun10 1), d3397–d3397. doi:10.1136/bmj.d3397

    Ultrasound Gallery

    Appendicitis

    Appendicitis

    Non-compressible tubular structure in the RLQ of a patient with focal abdominal tenderness. >6mm in diameter.

    Common Bile Duct

    Common Bile Duct

    A tubular structure typically anterior to the portal vein without flow. Normally measures <4mm, increases by 1mm per decade after 40yrs.

    Cellulitis

    Cellulitis

    "Cobblestone" appearance of soft tissue suggesting infection/edema.

    Fetal Heart Rate

    Fetal Heart Rate

    Placing the M-Mode marker over the most visibly active portion of the fetal heart allows for measurement of the fetal heart rate.

    Free Fluid

    Free Fluid

    Free fluid in the hepatorenal recess.

    Hydronephrosis

    Hydronephrosis

    Severe hydronephrosis.

    Thoracic Aorta Aneurysm

    Thoracic Aorta Aneurysm

    Subxiphoid view of thoracic aorta, markedly dilated (>3cm) with thrombus.

    Pericardial Effusion

    Pericardial Effusion

    Mild pericardial effusion in a patient with pleuritic chest pain.

    Inferior Vena Cava

    Inferior Vena Cava

    IVC without significant respiratory variation.

    B-lines

    B-lines

    B-lines extending deep from pleura suggestive of interstitial fluid accumulation (pulmonary edema).

    "Shred" sign

    "Shred" sign

    Irregular, "shredded" pleural line suggestive of consolidation.

    Pneumothorax

    Pneumothorax

    Transition point with loss of lung sliding in a patient with a small spontaneous pneumothorax.

    Lower Extremity Edema

    HPI:

    51 year-old male with a history of HTN, DM and chronic alcohol abuse presenting with lower extremity swelling. He notes one month of progressive, bilateral lower extremity swelling, in the past two weeks associated with increasing pain and redness and is now no longer able to ambulate due to pain. He denies fevers/chills, chest pain or shortness of breath. He also denies orthopnea and paroxysmal nocturnal dyspnea. He states that he has not had these symptoms prior to one month ago. On review of systems he denies nausea/vomiting, abdominal pain, and changes in bowel or urinary habits. He has a history of GI bleeding (unknown treatment) but denies hematemesis, hematochezia or melena. He has previously experienced alcohol withdrawal, which manifested as tremors, but no hallucinations or seizures.

    PMH:

    • HTN
    • DM
    • Chronic EtOH abuse

    PSH:

    None

    FH:

    Unknown

    SHx:

    • Drinks 1-2 pints of alcohol daily, last drink this morning.
    • Denies current tobacco or drug abuse, no prior IVDA.

    Meds:

    None

    Allergies:

    NKDA

    Physical Exam:

    VS: T 37.6 HR 86 RR 16 BP 128/84 O2 99% RA
    Gen: Adult, non-obese male, lying in bed. Tremors noted in upper extremities.
    HEENT: PERRL, EOMI, no scleral icterus. Mucous membranes moist.
    CV: RRR, normal S1/S2, no additional heart sounds, JVP 3cm above sternal angle at 30°.
    Lungs: CTAB, no crackles.
    Abd: Soft, non-distended, with normoactive bowel sounds. Liver edge palpated 1cm below costal margin at mid-clavicular line, non-tender. No rebound/guarding.
    Ext: Warm, well-perfused with 2+ distal pulses (PT, DP). 3+ pitting edema symmetric in bilateral lower extremities to knee. Erythema and warmth bilaterally extending from ankles to mid-shin. Mild tenderness to palpation. No pain with passive dorsiflexion. 3x3cm shallow ulceration below medial malleolus on right lower extremity without underlying fluctuance or expression of purulent material. No venous varicosities noted. Decreased sensation to light touch below knee bilaterally.
    Rectal: Normal rectal tone, brown stool, guaiac negative.
    Neuro: Alert and oriented, CN II-XII intact, gait intact, normal FTN/RAM.

    Labs/Studies:

    • CBC: 7.4/13.1/39/180
    • Creatinine: 0.84
    • Albumin: 4.3
    • BNP: 28

    Imaging:

    Venous Lower Extremity Ultrasound

    1. No DVT.
    2. Pulsatile flow in bilateral EIV (external iliac veins) suggestive of elevated right heart pressure.

    Assessment/Plan:

    51M with HTN, DM, EtOH abuse presenting with lower extremity edema. Chronic bilateral lower extremity edema likely secondary to chronic venous insufficiency perhaps related to OSA given ultrasound findings of pulsatile flow in EIV’s. Doubt systemic cause: no evidence of heart failure on exam and normal BNP, no stigmata of cirrhosis and normal albumin, normal creatinine. Also, no evidence of DVT on ultrasound though bilateral DVT unlikely. Bilateral cellulitis also unlikely as the patient is afebrile without leukocytosis, however the patient was started on antibiotics including ceftriaxone and TMP/SMX given erythema, warmth and tenderness to palpation. The patient received benzodiazepines which eased withdrawal symptoms and he was admitted for continued treatment.

    Mechanisms of Lower Extremity Edema: 1

    Mechanisms of Lower Extremity Edema

    Differential Diagnosis of Lower Extremity Edema: 1,2

    Differential Diagnosis of Lower Extremity Edema

    Evaluation:

    History 1,2

    • Duration: acute (<72h) vs. chronic
    • Pain: DVT, CRPS, less severe in venous insufficiency
    • Systemic Disease
      • Cardiac: orthopnea, PND
      • Renal: proteinuria
      • Hepatic: jaundice, ascites
    • Malignancy: lymphedema
    • Improvement with elevation/recumbency: venous insufficiency
    • OSA: snoring, daytime somnolence
    • Medications: B-blocker, CCB, hormones, NSAID’s

    Physical Exam 1,2

    • Distribution: unilateral, bilateral, generalized
    • Quality: pitting, non-pitting
    • TTP: DVT, cellulitis
    • Varicose veins: venous insufficiency
    • Kaposi-Stemmer: inability to pinch dorsum of foot at base of 2nd toe (lymphedema)
    • Systemic Disease
      • Cardiac: JVD, crackles
      • Hepatic: ascites, scleral icterus, spider angiomas
    • Brawny, medial maleolar involvement: venous insufficiency

    Key Features Distinguishing Cellulitis: 3

    • Typically unilateral and acute
    • Often with systemic symptoms (fever, leukocytosis)
    • Risk Factors: immunosuppression, previous episodes, DM, PVD

    References:

    1. Trayes, K. P., Studdiford, J. S., Pickle, S., & Tully, A. S. (2013). Edema: diagnosis and management. American family physician, 88(2), 102–110.
    2. Ely, J. W., Osheroff, J. A., Chambliss, M. L., & Ebell, M. H. (2006). Approach to leg edema of unclear etiology. Journal of the American Board of Family Medicine : JABFM, 19(2), 148–160.
    3. Keller, E. C., Tomecki, K. J., & Alraies, M. C. (2012). Distinguishing cellulitis from its mimics. Cleveland Clinic journal of medicine, 79(8), 547–552. doi:10.3949/ccjm.79a.11121
    4. WikEM: Pedal edema

    Lymphadenopathy Applied: Lymphoma

    HPI:

    27 year-old female with no medical history presenting with neck swelling. She describes one month of progressive enlargement of a left-sided neck mass, and in the past two weeks has noted a new right-sided neck mass. This has been associated with worsening dysphagia to solids, describing a sensation of food lodging in the mid-chest and requiring liquids for passage – she attributes her recent 10lb weight loss to this. She also reports a non-productive cough for the past two weeks and generalized fatigue. She otherwise denies fevers, night sweats, chest pain, shortness of breath, nausea/vomiting, or changes in bowel/urinary habits. She has no known sick contacts or TB exposure risk factors. She has no medical history, no prior surgeries, does not take any medications and denies tobacco, alcohol or drug use.

    Physical Exam:

    VS: T 38.4 HR 98 RR 14 BP 108/68 O2 99% RA
    Gen: Well-appearing young female, in no acute distress.
    HEENT: PERRL, EOMI, MMM without lesions. There is a 2x3cm firm, non-tender, mobile left supraclavicular lymph node, as well as two 1x1cm firm, non-tender lymph nodes in the left and right anterior cervical chains.
    CV: RRR, normal S1/S2, no murmurs. No JVD.
    Lungs: Clear to auscultation bilaterally. There is a transition to bronchial breath sounds along the trachea inferior to the sternal angle with normal tracheal sounds superiorly.
    Abd: Soft, non-tender without organomegaly.
    Ext: Warm and well-perfused with normal peripheral pulses. No axillary or inguinal lymphadenopathy.
    Neuro: Alert and oriented, responding appropriately to questions. PERRL, EOMI, facial sensation symmetric, facial muscles symmetric, hearing grossly normal, palate rises symmetrically, tongue movements normal without fasciculation, SCM/trapezius normal. Normal FTN, RAM. Gait intact. Peripheral sensation and motor grossly normal.

    Imaging:

    CT Chest - Axial

    CT Chest - Axial

    Anterior mediastinal mass with a wide differential - likely represents lymphoma or germ cell tumor. Less likely thymic or thyroid origin.

    CT Chest - Sagittal

    CT Chest - Sagittal

    Anterior mediastinal mass with a wide differential - likely represents lymphoma or germ cell tumor. Less likely thymic or thyroid origin.

    Assessment/Plan:

    27F with no PMH presenting with progressive localized lymphadenopathy. Resultant dysphagia, cervical and supraclavicular distribution as well as abnormal tracheal sounds concerning for mediastinal involvement. The patient is currently stable without evidence of airway compromise. A CT of the chest was obtained to evaluate for thoracic malignancy, which showed a large anterior mediastinal mass concerning lymphoma or germ cell tumor. The location of the mass likely explains the patient’s dysphagia due to compression of the esophagus, as well as the abnormal pulmonary exam with compression potentially irritating the trachea and triggering her non-productive cough. The patient was admitted for further workup.

    Lymphadenopathy Applied – Lymphoma

    This case applies the differential diagnosis of lymphadenopathy. The most abnormal finding on examination was non-tender, left supraclavicular lymphadenopathy. The duration of symptoms and lack of tenderness is concerning for malignancy, and the left supraclavicular location suggests a thoracic or intra-abdominal source.

    Lymphadenopathy Applied - Lymphoma

    Necrotizing Soft-Tissue Infection (NSTI)

    HPI:

    40 year-old male with a history of diabetes presents with right foot pain and swelling. His symptoms began 3 days ago with pain on the lateral surface of his right foot, described as aching, non-radiating and exacerbated with walking. Yesterday, he noted more prominent swelling and redness involving 4th and 5th toes. He denies trauma, fevers, and discharge.

    PMH:

    • Diabetes mellitus, diagnosed 8yrs ago

    PSH:

    • None

    FH:

    • Non-contributory

    SHx:

    • Lives with wife and 2 children and works an office job.
    • Ten year history of tobacco use, quit 3 years ago.
    • No EtOH or drug abuse.

    Meds:

    • Metformin 500mg p.o. b.i.d.
    • Ibuprofen p.r.n. joint pain

    Allergies:

    NKDA

    Physical Exam:

    VS: T 101.2 HR 88 RR 14 BP 147/71 O2 100% RA
    Gen: Obese male, pleasant and in no acute distress, lying in bed with right foot raised.
    HEENT: PERRL, EOMI, dry mucous membranes.
    CV: RRR, normal S1/S2, no extra heart sounds, no murmurs.
    Lungs: CTAB
    Abd: +BS, non-tender.
    Ext: Right lower extremity with 8x8cm area of erythema predominantly involving lateral aspect of foot, dorsum of foot and 3-5th digits. There is a shallow, 1x1cm ulcer on the plantar surface of foot near 5th MTP. Area is also notable for ecchymosis and palpable crepitus. There is minimal tenderness to palpation or with active/passive range of motion.
    Skin: The remainder of the skin exam is unremarkable.
    Neuro: AAOx3.

    Labs/Studies:

    • BMP: 134/4.3/104/26/18/1.4/206
    • WBC: 27.3/13.1/40/189 (90% neutrophils)
    • Lactate: 1.2
    • CRP: [pending]

    Imaging:

    CT Lower Extremity

    1. Calf cellulitis and gas-producing cellulitis in the lateral foot and toes.
    2. Thigh and inguinal lymphadenopathy.
    3. Although gas is seen down to the level of the bone, no definite bony changes are identified to establish a diagnosis of osteomyelitis. Please note that MRI is more sensitive for detection of early osteomyelitis.

    Assessment/Plan:

    40M with DM and diabetic foot ulcer resulting in a necrotizing soft tissue infection as evidenced by gas on imaging. Recommended surgical debridement and started on broad-spectrum antibiotics including:

    • vancomycin 1g i.v. q.12.h.
    • cefepime 2g i.v. q.8.h.
    • metronidazole 500mg i.v. q.8.h.

    The patient underwent amputation of 3-5th digits with good surgical margins and was discharged on post-operative day three in good condition.

    Skin and soft-tissue layers and their infections: 1

    Skin and soft-tissue layers and their infections

    Necrotizing Soft-Tissue Infections (NSTI):2,3,4

    Risk Factors

    • IVDA
    • Comorbid conditions
      • DM
      • Obesity
      • Immunosuppression

    Physical Exam

    • Early (non-specific)
      • Swelling
      • Erythema
      • Pain
    • Late (non-sensitive)
      • Tense edema outside affected skin perimeter
      • Disproportionate pain
      • Ecchymosis
      • Bullae
      • Crepitus
      • Systemic signs (fever, tachycardia, hypotension)

    Treatment

    • Surgical debridement
    • Antimicrobials
      • Carbapenem, combination B-lactam B-lactamase
      • Vancomycin, linezolid (MRSA coverage)
      • Clindamycin (inhibit protein synthesis)
    • Supportive therapy

    LRINEC score 5

    Name Value Score
    CRP ≥150 4
    WBC 15-25
    >25
    1
    2
    Hb 11-13.5
    <11
    1
    2
    Na <135 2
    Creatinine >1.6 2
    Glucose >180 1

    <5 Low risk, 6-7 Intermediate risk, >8 High risk

    References:

    1. Morchi, R. (2/18/14). Emergency Medicine Procedures Cadaver Lab. Clinical Clerkship at UCLA. Los Angeles, CA.
    2. Goldstein, E. J. C., Anaya, D. A., & Dellinger, E. P. (2007). Necrotizing Soft-Tissue Infection: Diagnosis and Management. Clinical infectious diseases, 44(5), 705–710. doi:10.1086/511638
    3. Headley, A. J. (2003). Necrotizing soft tissue infections: a primary care review. American family physician, 68(2), 323–328.
    4. McHenry, C. R., Piotrowski, J. J., Petrinic, D., & Malangoni, M. A. (1995). Determinants of mortality for necrotizing soft-tissue infections. Annals of surgery, 221(5), 558–63.
    5. Wong, C.-H., Khin, L.-W., Heng, K.-S., Tan, K.-C., & Low, C.-O. (2004). The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score: A tool for distinguishing necrotizing fasciitis from other soft tissue infections. Critical Care Medicine, 32(7), 1535–1541. doi:10.1097/01.CCM.0000129486.35458.7D

    Acute Respiratory Distress Syndrome

    HPI:

    25M with a history of mild asthma transferred from an outside hospital after 10 days in the intensive care unit for continued management of ARDS.

    The patient was well until one week prior to admission when he developed intermittent subjective fevers and general malaise associated with a non-productive cough and nausea/vomiting. He presented to the emergency department of an outside hospital with difficulty breathing and was noted to have respiratory distress and was subsequently admitted. Initial CT at the outside hospital revealed pneumomediastinum but no evidence of pulmonary embolism. Results from the outside hospital reveal a wide array of bacterial/fungal cultures and viral serologies including bronchoscopy but no obvious infectious source. The patient was treated with broad spectrum antibiotics for several days but his condition worsened requiring intubation, mechanical ventilation and transfer to the ICU. Further imaging was suggestive of ARDS, and the patient was transferred for additional management.

    The patient was well until one week prior to admission when he reported development of malaise and fatigue. On the day of hospitalization, the patient presented to primary care doctor with complaint of cough and shortness of breath and was found to be in respiratory distress and was admitted. The patient received IV antibiotics (cefepime, vancomycin) and was intubated when respiratory distress worsened. Found to have evidence of ARDS on CXR.

    PMH:

    • Mild asthma, not requiring medication
    • MRSA skin abscess

    PSH:

    • None

    FH:

    • Non-contributory.

    SHx:

    • Lives with family and works at a local supermarket. Rare alcohol use and no prior tobacco or drug use.
    • No recent travel or sick contacts.

    Meds:

    • ciprofloxacin 400mg i.v. q12h
    • linezolid 600mg i.v. q12h
    • meropenem 1g i.v. q8h
    • heparin 5000units s.q. q8h
    • cisatracurium 1.48mcg/kg/min
    • fentanyl 125mcg/hr
    • midazolam 10mg/hr
    • propofol 20mcg/kg/min

    Allergies:

    NKDA

    Physical Exam:

    VS: T 97.8 HR 120 RR 35 BP 123/68 O2 96%
    Vent: PRVC, VT 320, RR 35, PEEP 6, FiO2 95%
    Gen: Young male, thin-appearing, intubated and sedated and not responding to verbal commands
    HEENT: PERRL, unable to assess EOM, ET tube in place
    CV: RRR, normal S1/S2, no murmurs
    Lungs: Coarse breath sounds bilaterally
    Abd: Normoactive bowel sounds, soft, non-distended, no hepatosplenomegaly
    Ext: No clubbing, cyanosis, edema
    Neuro: Unable to assess

    Labs/Studies:

    • CBC: 25.06/7.0/21.3/426
    • BMP: 132/3.3/88/32/18/1.1/103
    • ABG: 7.30/97/76/18
    • Blood/sputum/urine cultures: Negative
    • Aspergillus, crypto, cocci: Negative
    • EBV, HIV, influenza, RSV: Negative

    Imaging


    CT Chest: Evidence of pneumomediastinum and pneumopericardium. Bilateral pulmonary infiltrates, but no pulmonary embolism.

    Assessment/Plan:

    25M with ARDS transferred from outside hospital for further management.
    # ARDS: Severe (P/F ratio <100). Etiology unclear, thorough infectious workup without obvious source. Consider autoimmune or allergic cause.

    • Ventilator: PRVC lung-protective ventilation
    • Consider NMB for dyssynchrony despite sedation
    • Monitor strict I/O, maintain net negative fluid balance.

    # Sepsis: Leukocytosis, tachycardia. Continue broad-spectrum antibiotics and monitor cultures.
    # Acidosis: Largely respiratory, place dialysis catheter if acute need arises.
    # Pneumomediastinum: Possible Boerhaave syndrome given reports of nausea/vomiting.

    Pathophysiology of Acute Respiratory Distress Syndrome (ARDS):1

    ARDS represents a stereotyped response to multiple insults. It is characterized by damaged capillary endothelium and alveolar epithelium resulting in increased permeability and the accumulation of fluid in the alveolar space. This causes diffuse alveolar damage and triggers the release of various cytokines (TNF, IL-1, IL-6) which recruit and activate neutrophils causing oxidative cell damage.

    Definition of ARDS (Berlin):2,3

    Timing Acute in onset (<1 week)
    Chest imaging Bilateral opacities
    Origin of pulmonary edema Not explained by heart failure or fluid overload (assessed with echocardiography)
    Oxygenation (PaO2/FiO2)
    1. Mild: 200-300
    2. Moderate: 100-200
    3. Severe: <100

    Causes of ARDS:2,4

    Causes of ARDS


    An Introduction to Mechanical Ventilation:5,6,7

    This is a simplification of the general principles underlying the most common ventilator modes. For more detail, see the articles cited in the references.
    An Introduction to Mechanical Ventilation

    Breath Sequences:

    Continuous Mandatory Ventilation (CMV)

    Continuous Mandatory Ventilation (CMV)

    All breaths controlled by ventilator, no triggered breaths.

    Assist-Control Ventilation (AC)

    Assist-Control Ventilation (AC)

    Every patient-triggered breath is fully supported, a backup rate is set. In the absence of patient-triggered breaths, AC acts like CMV.

    Synchronized Intermittent Mandatory Ventilation (SIMV)

    Synchronized Intermittent Mandatory Ventilation (SIMV)

    Preset minimum mandatory breaths are “synchronized” to patient’s efforts. The patient is allowed to breathe spontaneously between supported breaths.

    Pressure Support (PS)

    Pressure Support (PS)

    All breaths are triggered by the patient and each is supported by preset pressure.

    Continuous Positive Airway Pressure (CPAP)

    Continuous Positive Airway Pressure (CPAP)

    Spontaneous breathing at elevated baseline pressure.

    Control Variables:

    Volume Control (VC)
    Volume Control (VC)

    Volume Control (VC)

    Volume is set, pressure is variable. With a drop in compliance, the preset minimum volume is maintained with an increase in pressure.

    Pressure Control (PC)
    Pressure Control (PC)

    Pressure Control (PC)

    Pressure is set, volume is variable. With a drop in compliance, a smaller volume is delivered to maintain pressures at the preset limit.

    Pressure-Regulated Volume Control (PRVC)
    Pressure-Regulated Volume Control (PRVC)

    Pressure-Regulated Volume Control (PRVC)

    Pressure is targeted with a set minimum volume. The ventilator makes breath-to-breath adjustments of pressure to maintain minimum volumes. Breath mechanics are therefore comparable to pressure-control as a defined pressure is delivered based on prior breath’s respiratory mechanics (note pressure and flow tracings for PRVC/PC vs. VC)

    References:

    1. Pierrakos C, Karanikolas M, Scolletta S, Karamouzos V, Velissaris D. Acute respiratory distress syndrome: pathophysiology and therapeutic options. J Clin Med Res. 2012;4(1):7–16. doi:10.4021/jocmr761w.
    2. Fanelli V, Vlachou A, Ghannadian S, Simonetti U, Slutsky AS, Zhang H. Acute respiratory distress syndrome: new definition, current and future therapeutic options. J Thorac Dis. 2013;5(3):326–334. doi:10.3978/j.issn.2072-1439.2013.04.05.
    3. ARDS Definition Task Force, Ranieri VM, Rubenfeld GD, et al. Acute respiratory distress syndrome: the Berlin Definition. In: Vol 307. 2012:2526–2533. doi:10.1001/jama.2012.5669.
    4. Ware LB, Matthay MA. The acute respiratory distress syndrome. N. Engl. J. Med. 2000;342(18):1334–1349. doi:10.1056/NEJM200005043421806.
    5. Deng, J. (10/20/13). Principles of Mechanical Ventilation. Medical Intensive Care Unit Lecture. Los Angeles, CA.
    6. Singer BD, Corbridge TC. Basic invasive mechanical ventilation. South. Med. J. 2009;102(12):1238–1245. doi:10.1097/SMJ.0b013e3181bfac4f.
    7. Hamed HMF, Ibrahim HG, Khater YH, Aziz ES. Ventilation and ventilators in the ICU: What every intensivist must know. Current Anaesthesia & Critical Care. 2006;17(1-2):77–83. doi:10.1016/j.cacc.2006.07.008.

    Cervical Lymphadenopathy

    32 year-old male, previously healthy, with slowly-progressive right and left cervical lymphadenopathy over the past three years. He first noted the development of a mass on the lateral neck below the ear three years ago. This mass was non-tender and remained stable at approximately the size of a marble for nearly one year. He later developed more and larger masses, but never experienced any constitutional symptoms like fevers, night sweats, fatigue or weight loss. Examination reveals a healthy, well-nourished male with multiple, hard, mobile, non-tender right posterior cervical and submandibular lymph nodes and a large left supraclavicular lymph node, protruding above the clavicle and measuring ~4x3cm.

    Imaging:

    Cervical Lymphadenopathy - Axial

    Cervical Lymphadenopathy - Axial

    - Left supra-clavicular lymph node, 4.5 x 2.9 cm
    - Right posterior submandibular lymph node, 3.5 x 2.7 cm
    - Multiple other small cervical lymph nodes, more on the right

    Cervical Lymphadenopathy - Coronal

    Cervical Lymphadenopathy - Coronal

    - Left supra-clavicular lymph node, 4.5 x 2.9 cm
    - Right posterior submandibular lymph node, 3.5 x 2.7 cm
    - Multiple other small cervical lymph nodes, more on the right

    He has undergone several diagnostic procedures during this time including aspirations and core biopsies with inconclusive pathology and he is currently admitted for an excisional biopsy of the supraclavicular lymph node. Infectious and rheumatologic workup has remained negative including: HIV, bartonella, Quantiferon TB Gold, cocci, histo, toxo, CMV, EBV, ANA, RF, ACE.

    The patient tolerated the excisional biopsy without complication and was discharged. Preliminary pathology suggests Castleman’s disease.

    Lymph nodes and their drainage: 1,2

    Lymph Nodes of the Body
    Lymph Nodes of the Head and Neck

    Evaluation of Lymphadenopathy: 2,3,4

    Evaluation of Lymphadenopathy

    References:

    1. Ferrer R. Lymphadenopathy: differential diagnosis and evaluation. Am Fam Physician. 1998;58(6):1313–1320.
    2. Henry PH, Longo DL. Chapter 59. Enlargement of Lymph Nodes and Spleen. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson J, Loscalzo J. eds. Harrison’s Principles of Internal Medicine, 18e. New York: McGraw-Hill; 2012.
    3. Armitage JO. Chapter 171. Approach to the Patient With Lymphadenopathy and Splenomegaly In: Cecil, Russell L., Lee Goldman, and Andrew I. Schafer. Goldman’s Cecil medicine. Philadelphia: Elsevier/Saunders, 2011.
    4. Motyckova G, Steensma DP. Why does my patient have lymphadenopathy or splenomegaly? Hematol. Oncol. Clin. North Am. 2012;26(2):395–408– ix. doi:10.1016/j.hoc.2012.02.005.

    Hepatic Abscess

    HPI:

    42M with 1.5 weeks of fevers. Initially presented to ER 1wk ago and treated for possible otitis media, however follow-up ENT appointment showed no evidence of OM on exam. Fevers persisted and he developed headaches and went to urgent care where a CT head and LP were negative. A mild elevation of serum transaminases was noted and the following CT abdomen/pelvis was obtained. He denied GI symptoms.

    Imaging:

    Hepatic Abscess - Axial

    Hepatic Abscess - Axial

    - 7.4 cm cystic lesion in the inferior right lobe of the liver most consistent in appearance with hepatic abscess.
    - Multiple calcified gallstones with a 10 mm gallstone in the neck of the gallbladder or possibly in the cystic duct.

    Hepatic Abscess - Coronal

    Hepatic Abscess - Coronal

    - 7.4 cm cystic lesion in the inferior right lobe of the liver most consistent in appearance with hepatic abscess.
    - Multiple calcified gallstones with a 10 mm gallstone in the neck of the gallbladder or possibly in the cystic duct.

    Assessment & Plan:

    # Liver abscess: likely pyogenic s/p CT-guided drainage with 60cc purulent fluid removed. Gram stain showed GNR and WBC’s, culture grew Klebsiella pneumonia. Treated with ceftriaxone 2g IV q24h, metronidazole 500mg PO TID.

    Differential Diagnosis of Hepatic Abscess:1

    Differential Diagnosis of Hepatic Abscess

    References:

    1. Krige J, Beckingham IJ. Liver abscesses and hydatid disease. BMJ. 2001;322(7285):537–540.

    Volvulus


    Swirling mesenteric vessels in mid-pelvis associated with narrowed segments of small bowel and fluid-filled proximal small bowel raises concern for volvulus and small bowel obstruction.

    Alcoholic Hepatitis

    HPI:

    43 year-old female with a history of alcohol abuse and alcoholic hepatitis, presenting after referral from breast clinic for abnormal labs (notable for total bilirubin 18.1). The patient was well until two weeks ago when she noted increasing fatigue associated with morning nausea/vomiting (non-bloody) as well as yellowing of skin and eyes. She also reports darkening of urine, but no dysuria, change in volume of urine, or visible blood. She also denies fevers/chills, increased abdominal girth, abdominal pain, changes in bowel habits or bloody/dark stools.

    She reports drinking 1 pint of vodka daily for the past 15 years, and perhaps more in the past 3 weeks. Her last drink was in the morning on the day of admission, she denies any history of seizures and reports withdrawal symptoms (tremor, nausea) relieved with more alcohol. She currently denies anxiety/agitation, tactile/visual/auditory hallucinations.

    The patient was in breast clinic for evaluation of a painful breast mass which developed after biopsy of a lesion which was ultimately found to be benign. The patient noted the mass was growing in size and becoming more painful over the past month.

    PMH:

    • EtOH abuse
    • Alcoholic hepatitis

    PSH:

    • None

    FH:

    • No family history of breast/gynecologic malignancy.
    • Mother with history of stroke. Father with diabetes.

    SHx:

    • Lives alone.
    • Denies current or previous tobacco/drug use. Drinks 1 pint of whiskey daily for the past 15 years.
    • Not currently sexually active, no history of STI.

    Meds:

    • None

    Allergies:

    NKDA

    Physical Exam:

    VS: T 98.9 HR 104 RR 19 BP 117/67 O2 99% RA
    Gen: Well-appearing obese female in no acute distress
    HEENT: PERRL, marked scleral icterus, sublingual icterus, MMM, no lesions
    CV: Tachycardia, regular rhythm, normal S1/S2, no M/R/G
    Lungs: CTAB, no crackles/wheezing
    Abd: +BS, soft, non-distended, liver edge palpated 6cm below costal margin, irregular texture slightly tender to palpation, spleen not palpated, no fluid wave or shifting dullness, no rebound/guarding.
    Ext: Warm, well-perfused, 2+ pulses (DP/PT), slight yellowing.
    Skin: Vascular spiders on anterior chest, left breast with 5x5cm ecchymosis and tender underlying mass, no erythema, warmth, skin dimpling, nipple discharge.
    Neuro: AAOx4, CN II-XII intact, no tremor noted, gait normal.

    Labs/Studies:

    1mo prior to admission:

    • AST/ALT/AP/TB: 444/77/234/2.5

    Day 1:

    • AST/ALT/AP/TB: 185/61/184/18.1
    • PT/PTT/INR: 14.7/37.0/1.2

    Day 4:

    • AST/ALT/AP/TB: 142/50/153/25.5
    • PT/PTT/INR: 20.1/38.9/1.7

    Imaging:

    Abdominal US

    1. Markedly echogenic and enlarged liver with a nodular surface of cirrhosis.
    2. Markedly blunted hepatic vein waveforms commonly seen due to decreased hepatic parenchymal compliance although other etiologies causes of obstruction to hepatic venous outflow.
    3. Splenomegaly.

    Assessment/Plan:

    44F hx EtOH abuse, alcoholic hepatitis, presenting with acute alcoholic hepatitis.
    # Alcoholic hepatitis: Rapid onset of jaundice, tender hepatomegaly, and elevation of transaminases (AST > ALTx2) in the setting of chronic alcohol use suggestive of alcoholic hepatitis. Initial Maddrey discriminant hepatic function (mDH) score 37 suggestive of severe disease with high short-term mortality. Initiated trental 400mg p.o. t.i.d.
    # EtOH withdrawal: Last drink <24h ago, monitor for signs of withdrawal, treat with Ativan per withdrawal protocol. # Cirrhosis: Newly diagnosed on abdominal ultrasound. Complicated by coagulopathy, and likely portal hypertension given splenomegaly/thrombocytopenia. Plan for outpatient screening EGD and continued GI follow-up. # Breast mass: Likely hematoma 2/2 biopsy associated given increased size associated with progression of coagulopathy/thrombocytopenia. Outpatient ultrasound and follow-up scheduled. # Anemia: Macrocytic, potentially related to vitamin deficiency vs. bone-marrow suppression associated with chronic alcohol use. Start thiamine/folate/multivitamin. # FEN/GI/PPx: Encourage p.o. intake (2g sodium restriction), continue ondansetron p.r.n. nausea/vomiting, obtain nutrition consult.

    Hospital Course

    Patient’s liver function continued to decline as evidenced by worsening coagulopathy and increased serum bilirubin. mDH had increased to 58 by day four of hospitalization and steroids were added.

    Pathophysiology of Alcoholic Hepatitis: 1

    Ethanol promotes translocation of bacterial components (lipopolysaccharide) across the intestinal wall, into the portal venous system and liver. These trigger a local and systemic inflammatory response which leads to hepatocellular injury and systemic effects such as fever, anorexia and weight loss.

    Evaluation of Alcoholic Hepatitis: 1,2

    Clinical features:

    • Rapid onset jaundice
    • Tender hepatomegaly
    • Fever
    • Ascites
    • Proximal muscle loss
    • Encephalopathy

    Labs:

    • AST > ALT (x2), generally < 300IU/mL
    • Leukocytosis
    • ↑Total serum bilirubin
    • ↑INR
    • ↑Creatinine associated with poor prognosis

    Other studies:

    • Screening for infection: PNA, UTI, SBP
    • Abdominal US to evaluate hepatic abscess, HCC, extrahepatic biliary obstruction

    Management of Alcoholic Hepatitis: 1,2

    Grading Severity:

    • Maddrey’s discriminant function
    • Glasgow score
    • Lille score (assess response to corticosteroids after 1wk)

    Treatment:

    • Immediate and lifetime abstinence from alcohol
    • Trental 400mg p.o. t.i.d.
    • Prednisolone 40mg p.o. daily (controversial, some benefit in subgroup with Maddrey > 32)
    • Ascites: Sodium restriction, diuretics
    • Encephalopathy: Lactulose, rifaximin
    • Hepatorenal syndrome: albumin, vasopressors
    • Nutritional support

    Interpretation of Liver Function Tests: 3

    Disorder Bilirubin AST/ALT Albumin PT
    Hemolysis
    Gilbert
    ↑(indirect)
    No bilirubinuria
    Acute hepatocellular necrosis ↑ALT > AST
    > 500IU

    (poor prognosis if elevated)
    Chronic liver disease

    < 300IU

    Alcoholic hepatitis

    AST:ALT > 2

    Intra- extra-hepatic cholestasis

    < 500IU

    ↑↑

    (>4x normal)

    Features of Components of Liver Function Tests: 3,4

    Features of Components of Liver Function Tests

    References:

    1. Lucey, M. R., Mathurin, P., & Morgan, T. R. (2009). Alcoholic hepatitis. The New England journal of medicine, 360(26), 2758–2769. doi:10.1056/NEJMra0805786
    2. Sohail, U., & Satapathy, S. K. (2012). Diagnosis and management of alcoholic hepatitis. Clinics in liver disease, 16(4), 717–736. doi:10.1016/j.cld.2012.08.005
    3. Kaplan MM. Chapter 302. Evaluation of Liver Function. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012.
    4. Johnston, D. E. (1999). Special considerations in interpreting liver function tests. American family physician, 59(8), 2223–2230.

    Head Trauma: Radiographic Evolution

    CT Head (Initial)

    CT Head (Initial)

    - Noncontrast axial images through the head demonstrate no evidence of skull fracture.
    - Large lentiform-shaped mixed density extra-axial acute epidural hematoma in the right parietal occipital
    - Associated subdural hematoma tracking along right convexity toward the right temporal lobe.
    - There is no evidence of midline shift.

    CT Head (+8h)

    CT Head (+8h)

    - Significant interval increase in the size of the right hemispheric subdural hematoma
    - There is now midline shift from right to left at the level of the septum pellucidum measuring 10 mm, partial effacement of the right lateral ventricle and subfalcial herniation.
    - Scattered subarachnoid blood is redemonstrated.
    - Comminuted fractures of the nasal bone are present and there is overlying and associated periorbital soft tissue swelling.

    CT Head (+16h, s/p SDH evacuation)

    CT Head (+16h, s/p SDH evacuation)

    - Interval gross total evacuation of right hemispheric subdural hematoma.
    - Moderate anterior bifrontal subdural and right epidural air is present.
    - Small scattered subarachnoid and intraventricular blood is redemonstrated.

    Joint Pain and Tremor

    HPI:

    47 year-old female with a history of arthritis, gout and AVP (5/2013) resulting in tib/fib fracture s/p ORIF presenting with severe joint pain, worsening in the past week such that she has been unable to walk. While she reported significant diffuse joint pain, it was predominantly focused on her left leg, bilateral knees, and left shoulder. Joint pain progressively worsens over the course of the day and is worse with activity (better at rest). She reported occasional joint swelling, but no redness, fevers/chills, new trauma, recent travel, and is not sexually active. She reports suffering from joint pain for over 10 years, previously well-controlled with OTC pain medications (ibuprofen), however this had grown ineffective in the past week. She had been prescribed Norco after her surgery but was unable to afford it. She denies any recent intake of foods that have previously been triggers for acute gouty flares.

    PMH:

    • Arthritis
    • Gout

    PSH:

    • Left tib/fib fracture s/p ORIF

    FH:

    • No family history of RA, SLE or joint disease.

    SHx:

    • No t/e/d use
    • Lives at home alone

    Meds:

    • Ibuprofen 800mg p.o. p.r.n. pain

    Allergies:

    NKDA

    Physical Exam:

    VS: T 98.1 HR 109 RR 18 BP 108/66 O2 95% RA
    Gen: Thin female, appearing older than her stated age, in significant pain when helped to transfer to bed for examination
    HEENT: PERRL, MMM, no lesions
    CV: RRR, normal S1/S2, no M/R/G
    Lungs: CTAB, no crackles/wheezing
    Abd: +BS, soft, NT/ND, no masses
    Ext: Knees appear symmetric, no deformities, no erythema or warmth to touch, no effusion detected, significant tenderness to light touch of bilateral knees. Significant decreased ROM 2/2 pain in b/l lower extremities, limited to 30 degrees of knee flexion, unable to test strength 2/2 pain.Left lower extremity with 6cm longitudinal incisions on lateral and medial aspects of leg. Incisions appear well-healed without erythema/discharge. Decreased sensation on lateral and medial aspects of left leg.

    Left shoulder appears normal, no obvious deformities, no bony tenderness. Decreased ROM to 15 degrees of abduction/flexion/extension 2/2 pain.

    Neuro: AAOx4, CN II-XII intact, gait not tested. A high-frequency, high-amplitude tremor is noted in the bilateral upper extremities at rest and with activity. Tremor appears associated with patient’s distress and pain.

    Labs/Studies:

    • CBC: 9.4/12.8/38.1/311
    • BMP: 135/3.9/100/27/14/0.60/113
    • CRP: 0.18
    • ESRW: 20
    • Uric Acid: 2.6
    • XR Left Tibia/Fibula: There is a metallic fixation device noted in the tibia.  There is no evidence of loosening of the metallic components.  The bones appear to be in gross anatomic alignment.

    Assessment/Plan:

    47F w/hx arthritis, gout, recent tib/fib fx s/p ORIF presenting with worsening polyarticular arthralgia unresponsive to OTC medications admitted for evaluation and pain management.

    # Polyarticular arthralgia: Multiple joints affected, however patient notes most significant in bilateral knees and recently operated left leg. Polyarticular involvement, symmetric distribution and predominant involvement of large joints is suggestive of osteoarthritis. Also, given patient’s significant distress and multiple points of tenderness, potential extra-articular cause such as complex regional pain syndrome. Unlikely inflammatory arthritis (infectious, crystal arthropathy, rheumatic disease) given distribution and no significant erythema, warmth or effusion which could be aspirated. Obtained imaging of LLE to evaluate recent surgical repair of tib/fib fracture, with no evidence of loosening of fixation components or misalignment. Patient’s symptoms improved with morphine 5mg i.v. x2 in ED. Will admit for continued evaluation and pain management, consider addition of gabapentin for potential neuropathic pain associated with recent surgery.

    # Tremor: High-frequency, high-amplitude rest and action tremor suggestive of essential tremor or exaggerated physiological tremor associated with pain and emotional distress. No other neurological symptoms (HA, weakness) and non-focal neurological exam (aside from anesthesia localized around recent surgical incisions in LLE). Will continue monitoring, no need for imaging at this time.

    # Gout: Patient with history of gout, however, doubt that current arthralgia associated with acute gouty flare. Will continue monitoring exam and consider ortho consultation for joint aspiration.

    Differential Diagnosis of Monoarticular Arthralgia: 1,2

    Differential Diagnosis of Monoarticular Arthralgia

    Differential Diagnosis of Polyarticular Arthralgia 1,3

    Differential Diagnosis of Polyarticular Arthralgia

    Use of Serum Uric Acid in Acute Gout 4

    In this patient, serum uric acid levels were checked. However, a normal serum urate (SU) does not exclude an acute gout flare. Studies have shown 12-43% of patients with acute gout flares have normal SU. An elevated SU (>8.0mg/dL) may support the diagnosis of a gout flare but is not itself diagnostic.

    Approach to Joint Pain: 3

    Approach to Joint Pain

    Certain key historical elements can help narrow the differential diagnosis.

    1. Inflammation:
      1. Definition: Presence of erythema, warmth, swelling, pain with passive ROM, morning stiffness suggests inflammatory cause (arthritis)
      2. Common causes: Infection, gout, RA, SLE
    2. Chronology:
      1. Definition: Acute <6wks, chronic > 6wks
    3. Distribution:
      1. Definition: Location (large/small), symmetry
      2. Common causes:
        1. OA: DIP + PIP, spares wrists, elbows, ankles
        2. RA: PIP + MCP
        3. Spondylarthropathies (large joints)
        4. Symmetric involvement: RA, SLE
        5. Asymmetric involvement: Psoriatic arthritis, reactive arthritis, gout
    4. Course:
      1. Definition: Intermittent (gout), migrating (GC, Lyme, SLE)
    5. Demographics:
      1. Female <50: RA, SLE
      2. Male > 40: gout (♂ 20yr after puberty, ♀ 20yr after menopause)
    6. Extra-articular manifestations:
      1. Malar rash, oral ulcers: SLE
      2. Proximal muscle weakness: polymyositis
      3. Psoriatic skin/nail lesions: psoriatic arthritis
      4. Oral ulcers, vesicopustules on palms/soles, recent diarrheal illness: reactive arthritis

    Differential Diagnosis of Tremor: 5,6

    Differential Diagnosis of Joint Pain

    References:

    1. Cush JJ, Lipsky PE. Chapter 331. Approach to Articular and Musculoskeletal Disorders. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012. http://www.accessmedicine.com/content.aspx?aID=9139045. Accessed August 27, 2013.
    2. Siva, C., Velazquez, C., Mody, A., & Brasington, R. (2003). Diagnosing acute monoarthritis in adults: a practical approach for the family physician. American family physician, 68(1), 83–90.
    3. Mies Richie, A., & Francis, M. L. (2003). Diagnostic approach to polyarticular joint pain. American family physician, 68(6), 1151–1160.
    4. Schlesinger, N., Norquist, J. M., & Watson, D. J. (2009). Serum urate during acute gout. The Journal of rheumatology, 36(6), 1287–1289. doi:10.3899/jrheum.080938
    5. Hess, C. W., & Pullman, S. L. (2012). Tremor: clinical phenomenology and assessment techniques. Tremor and other hyperkinetic movements (New York, N.Y.).
    6. Crawford, P., & Zimmerman, E. E. (2011). Differentiation and diagnosis of tremor. American family physician, 83(6), 697–702.

    Hyperglycemic Crises

    CC:

    Blurred vision, numbness

    HPI:

    56 year-old male with a history of DM, questionable HTN presenting with blurred vision, numbness of fingertips/toes for 2wks. Associated symptoms include dry mouth, polydipsia/polyuria. He states that these symptoms coincide with elevated measurements of blood glucose at home (>500). He ran out of his diabetes medication (metformin) 8mo ago but states his BG was typically between 100-200 with diet/exercise until 2wks ago. He reports recent dietary indiscretions on a trip to Las Vegas.

    He denies fevers/chills, CP/SOB, cough, abdominal pain, N/V, or dysuria.

    PMH:

    • DM II
    • HTN

    PSH:

    None

    FH:

    Several maternal family members with DM.

    SHx:

    • No tobacco/drug use
    • 5-6 alcoholic drinks/wk

    Meds:

    • Metformin 500mg p.o. b.i.d.

    Allergies:

    NKDA

    Physical Exam:

    VS: T 37.8 HR 60 RR 14 BP 165/90 O2 99% RA
    Gen: Well-appearing, no acute distress, obese
    HEENT: PERRL, EOMI, optic discs sharp b/l, no abnormalities visualized
    CV: RRR, normal S1/S2, no M/R/G, no additional heart sounds
    Lungs: CTAB, no wheezes/crackles
    Abd: +BS, soft, NT/ND, no rebound/guarding
    Ext: Warm, well-perfused, 2+ pulses, no clubbing/cyanosis/edema
    Neuro: AAOx3, CN II-XII intact

    Labs/Studies:

    • BMP: 135/3.8/102/24/18/1.1/378
    • CBC: 7.4/14.1/42.0/403
    • UA: + glucose, – ketones

    Assessment/Plan:

    56M, hx DM with poor medication adherence presenting with vision changes and stocking/glove paresthesias for 2wks after reported dietary indiscretion found to be hyperglycemic. DKA/HHS unlikely given stable vital signs, normal metabolic panel with exception of isolated hyperglycemia (slight hyponatremia likely related to osmotic effect of elevated serum glucose). Also, no evidence of concerning precipitates for hyperglycemic crisis (no CP/SOB, no F/C, no cough, no abdominal pain, no change in mental status). Patient was discharged home with education on importance of medication adherence, refill of metformin, and follow-up with primary care physician for further management of DM and possible hypertension.

    Evaluation of hyperglycemic crises in patients with diabetes:1,2

    Evaluation of Hyperglycemic Crises in Patients with Diabetes

    Key signs/symptoms of HHS/DKA:

    • Both: Polyuria, polydipsia, weight loss, hypovolemia (dry MM, skin turgor, tachycardia, hypotension)
    • DKA: Short course (<24h), N/V, diffuse abdominal pain, Kussmaul respirations
    • HHS: Longer course (days/weeks), altered mental status (lethargy, coma, seizure)

    Admission Laboratory Data of Patients with HHS vs. DKA:1

    DKA HHS
    Glucose (mg/dl) 616 930
    pH 7.12 7.30
    3-β-hydroxybutyrate (mmol/l) 9.1 1.0
    Serum osmolality 323 380
    Delta gap (AG-12) 17 11
    Na (mEq/l) 134 149
    K (mEq/l) 4.5 3.9
    Bicarbonate (mEq/l) 9 18

    References:

    1. Kitabchi, A. E., Umpierrez, G. E., Miles, J. M., & Fisher, J. N. (2009). Hyperglycemic crises in adult patients with diabetes. Diabetes care, 32(7), 1335–1343. doi:10.2337/dc09-9032
    2. De Beer, K., Michael, S., Thacker, M., Wynne, E., Pattni, C., Gomm, M., Ball, C., et al. (2008). Diabetic ketoacidosis and hyperglycaemic hyperosmolar syndrome – clinical guidelines. Nursing in critical care, 13(1), 5–11. doi:10.1111/j.1478-5153.2007.00259.x
    3. Stoner, G. D. (2005). Hyperosmolar hyperglycemic state. American family physician, 71(9), 1723–1730.

    Angioedema

    AngioedemaHPI:

    63-year old African American male with a history of HTN presenting with lip swelling x1 day. The patient states he was well until this morning when he noticed progressive swelling of his lips. The swelling is not associated with any difficulty speaking, swallowing or breathing and is not painful.

    He denies new rashes or itching, and has no history of such swelling. He also denies any exposure to known allergens, recent insect bites or travel. He has been taking lisinopril for his blood pressure regularly for the past several months and denies any prior adverse effects (cough, rash).

    PMH:

    • Parkinson Disease
    • HTN

    PSH:

    None

    FH:

    No family history of angioedema

    SHx:

    • No t/e/d use
    • Lives at home with caretaker

    Meds:

    • Lisinopril 20mg p.o. daily
    • Carbidopa/levodopa 50mg p.o. t.i.d.

    Allergies:

    NKDA

    Physical Exam:

    VS: T 37.8 HR 84 RR 14 BP 146/98 O2 99% RA
    Gen: Well-appearing, no respiratory distress, speaking comfortably
    HEENT: PERRL, significant external upper/lower lips swelling extending to lateral cheeks, non-tender, no fluctuance or overlying skin changes. No visible tongue swelling, floor of mouth swelling/tenderness, uvular/palatal deviation.
    CV: RRR, no M/R/G
    Lungs: CTAB, no crackles/wheezing, good air movement b/l
    Abd: +BS, soft, NT/ND, no rebound/guarding
    Ext: Warm, well-perfused, 2+ peripheral pulses
    Skin: No visible skin lesions/rashes
    Neuro: AAOx4, CN II-XII intact

    Assessment/Plan:

    63M with acute onset, progressive facial swelling. Currently restricted to external lips, with no evidence of airway compromise. Likely ACE inhibitor-induced angioedema given patient is on lisinopril and has no history of hereditary angioedema. Doubt anaphylaxis given no allergies, suspicious exposures or history of pruritus. Doubt infection given afebrile and painless swelling without e/o erythema.

    Pathophysiology of ACE inhibitor-induced angioedema1

    Pathophysiology of ACE-inhibitor induced angioedema

    Angioedema is a vascular reaction associated with tissue (subcutaneous, submucosal) edema resulting from increased activity of vasoactive substances. The vasoactive substances in ACE inhibitor-induced angioedema are bradykinin and substance P. In the presence of ACE inhibition, these enzymes are inactivated through alternative pathways which, if disturbed, lead to angioedema.

    Epidemiology of ACE inhibitor-induced angioedema

    Angioedema occurs in 0.1-0.7% of patients taking ACE inhibitors, and 60% of cases occur within the first week of starting an ACE inhibitor (though it can occur as much as years later).2,3 ACE inhibitors are implicated as the cause of 20-40% of all ED visits for angioedema.4

    Risk Factors2,5,6

    • Female
    • Age > 65yo
    • African American
    • Prior angioedema
    • Smoking
    • ACE inhibitor-associated cough

    Clinical Features of ACE inhibitor-induced angioedema

    Affected Sites:

    • Mucous membranes of the head and neck
      • Face
      • Tongue
      • Lips
      • Pharynx
      • Larynx
    • GI tract
      • Diffuse abdominal pain
      • Nausea/vomiting/diarrhea

    Signs/Symptoms at initial presentation:4

    • SOB (89%)
    • Lip swelling (70%)
    • Tongue swelling (52%)
    • Voice change/hoarseness (29%)
    • Stridor (11%)

    Key Clinical Features:

    • Onset in minutes with resolution in 24-72 hours
    • Absence of itching/urticaria7

    Staging and Disposition:8

    Stage Affected Site Outpatient (%) Floor (%) ICU (%) Intervention (%)
    I Face, lip 48 52 0 0
    II Soft palate 60 40 0 0
    III Tongue 26 7 67 7
    IV Larynx 0 0 100 24

    Management of ACE inhibitor-induced angioedema

    • Proven benefit
      • Airway management
      • Withdrawal of ACE inhibitor
    • Unclear benefit
      • Epinephrine 0.3mg IM q15min
      • Diphenhydramine 50mg IV
      • Famotidine 20mg IV
      • Solumedrol 125mg IV
    • Future treatment options
      • FFP: contains ACE9
      • Icatibant: bradykinin B2 receptor antagonist10,11

    References:

    1. Vleeming, W., van Amsterdam, J. G., Stricker, B. H. C., & de Wildt, D. J. (1998). ACE inhibitor-induced angioedema. Drug Safety, 18(3), 171–188. doi:10.2165/00002018-199818030-00003
    2. Grant, N. N., Deeb, Z. E., & Chia, S. H. (2007). Clinical experience with angiotensin-converting enzyme inhibitor-induced angioedema. Otolaryngology – head and neck surgery, 137(6), 931–935. doi:10.1016/j.otohns.2007.08.012
    3. Slater, E. E., Merrill, D. D., Guess, H. A., Roylance, P. J., Cooper, W. D., Inman, W. H., & Ewan, P. W. (1988). Clinical profile of angioedema associated with angiotensin converting-enzyme inhibition. JAMA : the journal of the American Medical Association, 260(7), 967–970.
    4. Banerji, A., Clark, S., Blanda, M., LoVecchio, F., Snyder, B., & Camargo, C. A. (2008). Multicenter study of patients with angiotensin-converting enzyme inhibitor-induced angioedema who present to the emergency department. Annals of allergy, asthma & immunology, 100(4), 327–332. doi:10.1016/S1081-1206(10)60594-7
    5. Gibbs, C. R., Lip, G. Y., & Beevers, D. G. (1999). Angioedema due to ACE inhibitors: increased risk in patients of African origin. British journal of clinical pharmacology, 48(6), 861–865.
    6. Morimoto, T., Gandhi, T. K., Fiskio, J. M., Seger, A. C., So, J. W., Cook, E. F., Fukui, T., et al. (2004). An evaluation of risk factors for adverse drug events associated with angiotensin-converting enzyme inhibitors. Journal of evaluation in clinical practice, 10(4), 499–509. doi:10.1111/j.1365-2753.2003.00484.x
    7. Kanani, A., Schellenberg, R., & Warrington, R. (2011). Urticaria and angioedema. Allergy, Asthma & Clinical Immunology, 7(Suppl 1), S9. doi:10.1186/1710-1492-7-S1-S9
    8. Ishoo, E., Shah, U. K., Grillone, G. A., Stram, J. R., & Fuleihan, N. S. (1999). Predicting airway risk in angioedema: staging system based on presentation. Otolaryngology – head and neck surgery, 121(3), 263–268.
    9. Hassen, G. W., Kalantari, H., Parraga, M., Chirurgi, R., Meletiche, C., Chan, C., Ciarlo, J., et al. (2013). Fresh frozen plasma for progressive and refractory angiotensin-converting enzyme inhibitor-induced angioedema. The Journal of emergency medicine, 44(4), 764–772. doi:10.1016/j.jemermed.2012.07.055
    10. Bas, M., Greve, J., Stelter, K., Bier, H., Stark, T., Hoffmann, T. K., & Kojda, G. (2010). Therapeutic Efficacy of Icatibant in Angioedema Induced by Angiotensin-Converting Enzyme Inhibitors: A Case Series. Annals of emergency medicine, 56(3), 278–282. doi:10.1016/j.annemergmed.2010.03.032
    11. MD, M. G., & MD, M. A. (2012). Icatibant: a novel approach to the treatment of angioedema related to the use of angiotensin-converting enzyme inhibitors. American Journal of Emergency Medicine, 30(8), 1664.e1–1664.e2. doi:10.1016/j.ajem.2011.09.014

    Hearing loss and Tinnitus

    HPI:

    42 year-old male with no significant medical history presenting to ENT clinic after referral from PMD for perforated TM. The patient last had normal hearing approximately 1yr ago when he noted acute onset of right ear pain, discharge, hearing loss and ringing in the setting of fever and a productive cough. He does not recall an inciting event (trauma, swimming) to this initial episode, and had no previous history of ear infections. He saw his PMD several days later, was told he had a perforated ear drum and was treated with antibiotics.

    Since then, the patient has not had any further ear pain or discharge but is left with persistent and constant hearing loss and ringing (high-pitched, non-pulsatile).

    PMH:

    None

    PSH:

    None

    FH:

    Non-contributory

    SHx:

    Worked in construction for 20yrs

    Meds:

    None

    Allergies:

    NKDA

    Physical Exam:

    Gen: Well-appearing, no acute distress
    Head: NC/AT
    Eyes: PERRL (4-2mm), disc margins sharp
    Ears: Weber lateralizes to left, AC > BC b/l
    AD: Decreased acuity to finger rub, EAC with some cerumen, cleared to reveal central perforation in posterior-superior quadrant of tympanic membrane.
    AS: EAC clear, TMI
    Nose: Nasal mucosa pink, septum midline
    Mouth: MMM, no lesions, good dentition, no pharyngeal erythema/exudates
    Neck: Trachea midline, supple, no cervical lymphadenopathy, no thyroid enlargement

    Studies

    Audiogram

    Audiogram: Severe low-mid frequency progressing to profound high frequency mixed hearing loss

    Assessment/Plan:

    42M, no significant PMH, with perforated TM and audiogram showing mixed hearing deficit. The patient describes a history suggestive of acute otitis media complicated by TM perforation. Persistent perforation seen on examination today can result in the tinnitus and hearing loss the patient complains of. However the marked sensorineural component remains unexplained, particularly given the patient reported previously normal hearing. While there is some evidence that acute otitis media can lead to sensorineural hearing loss, it is typically only mild and only in high-frequency ranges.1,2  Plan for further evaluation with repeat audiogram and MRI IAC, RTC when studies completed.


    Examination of the Ear3

    1. External Auditory Canal: in acute otitis externa, the canal will be narrowed, swollen and erythematous
    2. Tympanic Membrane: use cone of light for orientation, identify malleus and move speculum to visualize all four quadrants
    Tympanic Membrane
    Ear Anatomy
    Normal
    Perforation
    Tympanosclerosis
    Acute Otitis Media

    Differential Diagnosis of Hearing Loss4

    Differential Diagnosis of Hearing Loss

    Differential Diagnosis of Tinnitus5

    Differential Diagnosis of Tinnitus

    References:

    1. Tarlow, M. (1998). Otitis media: pathogenesis and medical sequelae. Ear, nose, & throat journal, 77(6 Suppl), 3–6.
    2. Tsuprun, V., Cureoglu, S., Schachern, P. A., Ferrieri, P., Briles, D. E., Paparella, M. M., & Juhn, S. K. (2008). Role of pneumococcal proteins in sensorineural hearing loss due to otitis media. Otology & neurotology, 29(8), 1056–1060.
    3. Bickley, Lynn S., Peter G. Szilagyi, and Barbara Bates. Bates’ guide to physical examination and history taking. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2009. Print.
    4. Isaacson, J. E., & Vora, N. M. (2003). Differential diagnosis and treatment of hearing loss. American family physician, 68(6), 1125–1132.
    5. Crummer, R. W., & Hassan, G. A. (2004). Diagnostic approach to tinnitus. American family physician, 69(1), 120–126.

    Dysphonia (Hoarseness)

    Case 1

    HPI:

    36 year-old female with no significant medical history who presents after referral for voice hoarseness. According to the patient, she underwent a C-section 3 months ago (at an outside hospital) complicated by bleeding requiring a second operation (L salpingoophorectomy); however, neither procedure required emergent intubation. She reports that she had some vomiting associated with anesthesia which ultimately required intubation and admission to the MICU for 5-6d. She was discharged 10 days after the initial operation, and both she and her baby were in good health. Two weeks after discharge, she began experiencing throat irritation and 1 month after discharge she noticed voice hoarseness which has been persistent. Today, she denies difficulty swallowing or breathing, F/C, N/V, abdominal pain.

    PMH:

    None

    PSH:

    Cesarean x2, L salpingoophorectomy

    FH:

    Non-contributory

    SHx:

    Lives at home taking care of 3 children, denies t/e/d

    Meds:

    None

    Allergies:

    NKDA

    Physical Exam:

    Gen: WA, NAD
    Head: NC/AT
    OC: MMM, no lesions, no pharyngeal erythema/exudates, hoarse voice
    Ears: EAC clear, TMI b/l
    Flex: Posterior commissure edema, cobblestoning, b/l TVC with shiny white masses
    Flexible nasolaryngoscopy image showing trauma granulomata.

    Flexible nasolaryngoscopy image showing trauma granulomata.

    Assessment/Plan:

    36F, no significant PMH, recent Cesarean and L salpingoophorectomy c/b likely aspiration requiring intubation and mechanical ventilation for several days with onset of progressive voice hoarseness 1mo later. History and flexible nasolaryngoscopy consistent with trauma granulomata, as well as laryngopharyngeal reflux.

    • Discussed treatment options with patient, recommend voice rest x2mo and continued monitoring
    • Laryngopharyngeal reflux, given dietary/lifestyle education, start omeprazole 20mg p.o. b.i.d.
    • RTC 1mo

    Case 2

    HPI:

    51 year-old female with a history of Hepatitis C, COPD and an 80 pack-year smoking history presents with concern about progressive voice hoarseness x2mo. She reports quitting smoking two months ago and is not sure if the hoarseness preceded or followed quitting. She has occasional throat discomfort which is mild. She otherwise denies difficulty or pain with swallowing, worsening shortness of breath, unintentional weight loss.

    She also reports a new mass on her neck which she first noticed yesterday. Denies associated pain, or surrounding skin changes.

    PMH:

    • Hepatitis C
    • COPD

    PSH:

    • Hysterectomy

    FH:

    Non-contributory

    SHx:

    80 pack-year smoking history, no current EtOH, drug use (previously used heroin and opiates)

    Meds:

    • Methadone
    • Elavil
    • Multiple unknown inhaled medications

    Allergies:

    • Naproxen (swelling)

    Physical Exam:

    Gen: WA, NAD
    Head: NC/AT
    Eyes: PERRL, EOMI
    Ears: b/l EAC erythema, TMI, no lesions/exudates
    OC: MMM, no lesions
    Neck: Supple, no thyroid enlargement, no cervical lymphadenopathy, 5x6cm soft, round, mobile, non-tender mass on left lateral neck w/o overlying skin changes
    Flex: Diffuse laryngeal damage, thickened posterior commissure, right TVC with area of leukoplakia, left TVC appears irregular

    Assessment/Plan:

    51F hx HepC, COPD, 80py smoking, presenting with voice hoarseness x2mo. History concerning for malignancy, exam today shows significant laryngeal damage and vocal cord irregularities warranting further evaluation. Possible component of fungal infection 2/2 inhaled steroid use for COPD, plan to reduce potentially aggravating factors (treat fungal infection, voice rest) and repeat evaluation. Neck mass possibly lipoma however will evaluate further given concern for malignancy.

    • Start fluconazole 100mg two tables p.o. on day1, 100mg p.o. daily x7d
    • Start nystatin 100,000 units/mL 10mL gargle and swallow t.i.d. x2wks
    • Advised voice rest
    • RTC in 3wks
    • CT neck/soft tissue w/wo IV contrast to evaluate neck mass

    Anatomy of the Pharynx/Larynx:

    Vocal cord anatomy
    Pharyngeal wall anatomy
    Structure of the pharynx

    Physiology of Voice Production: 1

    Voice is produced through the passive vibration of vocal folds in an air stream and requires:

    1. Adequate Air Stream
    2. Smooth vocal fold edges
    3. Vocal folds with normal vibratory properties
    4. Appropriate vocal fold positioning

    Differential diagnosis of dysphonia (hoarseness): 1,2,3

     Differential Diagnosis of Dysphonia (hoarseness)

    Characteristics of Hoarse Voice: 5

    Characteristic Likely cause
    Breathy Vocal cord paralysis
    Hoarse Vocal cord lesion, LPR
    Low-pitched Reinke’s edema, vocal abuse, LPR

    References:

    1. Mau, T. (2010). Diagnostic Evaluation and Management of Hoarseness. Medical Clinics of North America, 94(5), 945–960. doi:10.1016/j.mcna.2010.05.010
    2. Feierabend, R. H., & Shahram, M. N. (2009). Hoarseness in adults. American family physician, 80(4), 363–370.
    3. Schwartz, S. R., Cohen, S. M., Dailey, S. H., Rosenfeld, R. M., Deutsch, E. S., Gillespie, M. B., Granieri, E., et al. (2009, September). Clinical practice guideline: hoarseness (dysphonia). Otolaryngology. doi:10.1016/j.otohns.2009.06.744
    4. Bruch, J.W., Kamani D.V. Diaphragmatic pacing. In: UpToDate, Basow, DS (Ed), UpToDate, Waltham, MA, 2013.
    5. Rosen, C. A., Anderson, D., & Murry, T. (1998). Evaluating hoarseness: keeping your patient’s voice healthy. American family physician, 57(11), 2775–2782.

    Elevated Hemidiaphragm

    CXR - PA
    CXR - Lateral

    Causes of an Elevated Hemidiaphragm

    Causes of an elevated hemidiaphragm

    References:

    1. Lavender, JP, Potts DG (1959). Differential diagnosis of elevated right diaphragmatic dome. The British journal of radiology, 32(373), 56–60.
    2. Nason, L. K., Walker, C. M., McNeeley, M. F., Burivong, W., Fligner, C. L., & Godwin, J. D. (2012). Imaging of the diaphragm: anatomy and function. Radiographics : a review publication of the Radiological Society of North America, 32(2), E51–70. doi:10.1148/rg.322115127
    3. Prokesch, R. W., Schima, W., & Herold, C. J. (1999). Transient elevation of the hemidiaphragm. The British journal of radiology, 72(859), 723–724.
    4. Burgener, F., Kormano, M. & Pudas, T. (2008). Differential diagnosis in conventional radiology. Stuttgart New York: Thieme.

    Renal Failure in Cirrhosis

    CC:

    Consult for acute kidney injury

    HPI:

    63M with a history of liver cirrhosis of cryptogenic etiology, portal vein thrombosis, and esophageal varices s/p banding (2011) who was admitted to an OSH for altered mental status and hypotension requiring dopamine and was transferred to this facility for a higher level of care.

    The nephrology service was consulted for elevated serum creatinine concerning for AKI. The patient has a baseline creatinine of 1.1 (3/2013), 1.9 on transfer and continued worsening to peak of 2.6 today.

    PMH:

    • Asthma
    • COPD
    • Cirrhosis (PVT, encephalopathy)
    • Inguinal hernia (recurrent)

    PSH:

    • Appendectomy
    • Bilateral inguinal hernia repair

    FH:

    • Non-contributory

    SHx:

    • Married
    • Denies t/e/d use

    Meds:

    • albumin 25g i.v. q.6.h.
    • erythromycin 1,000mg p.o. q.1.h.
    • fluticasone-salmeterol 1 puff b.i.d.
    • lactulose 45g p.o. q.6.h.
    • neomycin 1,000mg p.o. q.1.h.
    • pantoprazole 40mg i.v. daily
    • rifaximin 550mg p.o. b.i.d.
    • sodium benzoate 5g p.o. b.i.d.

    Allergies:

    • Sulfa

    Physical Exam:

    VS: T 37.4 HR 90 RR 15 BP 86/48 O2 97% RA
    Gen: Chronically ill-appearing.
    HEENT: PERRL, scleral icterus, MMM
    CV: RRR
    Lungs: CTAB
    Abd: +BS, soft, non-tender, non-distended
    GU: Large ascites filled scrotum, testicles/inguinal canal not easily palpated
    Ext: Warm, well-perfused
    Skin: No palmar erythema, no vascular spiders
    Neuro: AAOx4, CN II-XII grossly intact

    Labs:

    • BMP: 134/4.5/103/20/41/3.0/106 (Ca 9.3, Mg 3.7, PO4 2.4)
    • LFT: AST 89, ALT 33, TB 26.6, CB 16.1, Alb 2.7
    • NH4 167

    Imaging:

    Pleural Effusion

    Pleural Effusion

    Large right pleural effusion with underlying compressive atelectasis.

    Cirrhosis and Portal Hypertension

    Cirrhosis and Portal Hypertension

    Shrunken/nodular liver with sequelae of portal hypertension including perisplenic collaterals, and splenomegaly.

    SMV Thrombosis

    SMV Thrombosis

    Near-total thrombosis of the portal vein extending down to superior mesenteric vein.

    B/L Inguinal Hernias

    B/L Inguinal Hernias

    Large volume abdominal ascites with a large amount of fluid extending into the bilateral inguinal canals.

    Large Right Inguinal Hernia

    Large Right Inguinal Hernia

    Large volume abdominal ascites with a large amount of fluid extending into the bilateral inguinal canals.

    CT Abdomen/Pelvis (PVT)

    CT Abdomen/Pelvis (PVT)

    Assessment/Plan:

    63M with a history of liver cirrhosis of cryptogenic etiology, recently with hypotension prior to transfer to this facility and increase in creatinine from 1.9-3.0 on current admission (from baseline 1.1).

    These findings indicate acute kidney injury, likely hepatorenal syndrome vs. acute tubular necrosis 2/2 prolonged hypotension. Plan to discontinue diuretics and start albumin challenge (1g/kg/day divided q6h x2d). Will also check UA, urine Na/cr/urea/eos, renal US (evaluate obstruction, kidney size). Start midodrine/octreotide for underlying HRS.

    1. Neuro: Intermittent confusion. Lactulose, rifaximin, benzoate.
    2. Resp: 2L NC. ABG 7.36/51/87/27.7/+2. CXR: Large R effusion.
    3. CV: Levo 0.075. Midodrine 15 TID. MAPs 60, HR 80s.
    4. GI: NPO/NGT. TPN.
    5. Renal: See above.
    6. Heme: Coagulopathy, keep INR <2.5
    7. ID: Afebrile. No abx.
    8. Endo: Euglycemic

    Renal Failure in Cirrhosis:

    Renal failure in cirrhosis is associated with higher mortality both before and after transplant. The main causes of renal failure in cirrhosis are detailed below, with particular attention to an entity unique to cirrhosis: the hepatorenal syndrome.1

    Disorder Pathogenesis Diagnosis Management
    HRS Dilation of splanchnic arteries initially compensated by increased CO eventually decompensates with activation of mechanisms to preserve ECBV (RAAS, SNS, ADH) leading to fluid retention (ascites, edema) and renal failure due to intrarenal vasoconstriction.Bacterial translocation and the resulting inflammatory response may contribute to splanchnic vasodilation (through production of vasoactive factors like NO).
    • Serum creatinine > 1.5mg/dl-  Not reduced with 1g/kg albumin
    • No confounding factors (2d off diuretics, no nephrotoxic agents, no shock, no e/o intrinsic renal disease)
    • Type 1: doubling creatinine > 2.5mg/dL in <2wk
    • Type 2: stable, slower progression
    • Vasoconstrictor therapy-  Albumin
    • Portasystemic shunting
    • Renal replacement therapy
    • Prevention
      • Norfloxacin
      • Albumin
    Intrinsic renal Some causes of liver disease are also associated with intrinsic renal pathology (ex. GN associated with HBV, HCV).
    • Proteinuria, hematuria
    • Renal bx
    • Active urinary sediment
    • Antiviral therapy if appropriate
    Pre-renal AKI Hemorrhage (GIB), fluid losses (excess diuresis, diarrhea from lactulose).
    • Suspected from patient history
    • Low FENa, bland urine sediment
    • Hemorrhage: replace volume with fluids, blood products. Control bleeding.
    • Discontinue diuretics, administer fluids if tolerated
    ATN Severe ischemic or toxic (NSAID’s, nephrotoxic medications)
    • Renal tubular epithelial cells favor ATN (granular casts common in ATN, HRS)
    • Withdraw therapy
    • Avoid nephrotoxic agents

    Pathophysiology of Hepatorenal Syndrome:

    Pathophysiology of Hepatorenal Syndrome

    Evaluation:

    The evaluation of suspected renal failure in patients with cirrhosis involves assessment of renal function for evidence of acute impairment, as well as analaysis of urine for protein or active sediment to suggest intrinsic renal disease (possibly warranting renal ultrasonography or biopsy). Additionally, patients should be evaluated for evidence of bacterial infection including assessment of ascites if present as SBP produces a more severe form of the inflammatory vasodilation mechanism suspected to play a role in HRS.

    Treatment:

    For renal failure not caused by the hepatorenal syndrome, identification and management of the underlying cause is critical (intrinsic renal disease, hypovolemia/hemorrhage, nephrotoxicity, infection). For suspected HRS, management is dependent on the acuity and setting. In the intensive care unit, vasoconstrictor therapy (norepinephrine, vasopressin) in association with albumin is effective in the treatment of HRS.2,3  In less acute settings, a combination of midodrine, octreotide and albumin improves renal function and is associated with lower short-term mortality.4 Alternatives for patients who do not respond to medical therapy include TIPS, dialysis and transplant.

    Summary:

    Renal failure in ESLD is due to the causes, complications or management of cirrhosis and has important implications, with HRS in particular offering the worst prognosis.5 Early recognition and management is critical to improving outcomes.

    References:

    1. Ginès, P., & Schrier, R. W. (2009). Renal failure in cirrhosis. The New England journal of medicine, 361(13), 1279–1290. doi:10.1056/NEJMra0809139
    2. Singh, V., Ghosh, S., Singh, B., Kumar, P., Sharma, N., Bhalla, A., Sharma, A. K., et al. (2012). Noradrenaline vs. terlipressin in the treatment of hepatorenal syndrome: a randomized study. Journal of hepatology, 56(6), 1293–1298. doi:10.1016/j.jhep.2012.01.012
    3. Kiser, T. H., Fish, D. N., Obritsch, M. D., Jung, R., MacLaren, R., & Parikh, C. R. (2005). Vasopressin, not octreotide, may be beneficial in the treatment of hepatorenal syndrome: a retrospective study. Nephrology, dialysis, transplantation, 20(9), 1813–1820. doi:10.1093/ndt/gfh930
    4. Esrailian, E., Pantangco, E. R., Kyulo, N. L., Hu, K.-Q., & Runyon, B. A. (2007). Octreotide/Midodrine therapy significantly improves renal function and 30-day survival in patients with type 1 hepatorenal syndrome. Digestive diseases and sciences, 52(3), 742–748. doi:10.1007/s10620-006-9312-0
    5. Alessandria, C., Ozdogan, O., Guevara, M., Restuccia, T., Jiménez, W., Arroyo, V., Rodés, J., et al. (2005). MELD score and clinical type predict prognosis in hepatorenal syndrome: relevance to liver transplantation. Hepatology (Baltimore, Md.), 41(6), 1282–1289. doi:10.1002/hep.20687

    Macroscopic Hematuria

    CC:

    Macroscopic hematuria

    HPI:

    85yo male with a history of prostate cancer s/p radiation and androgen deprivation therapy four years ago complicated by urethral strictures requiring chronic indwelling catheter who presented to the ED yesterday with 3 days of red urine followed by no output from catheter and abdominal pain. In the ED, the patient was found to have stable hemoglobin and creatinine and was discharged with urology follow-up after symptom resolution with catheter irrigation.

    Today, the patient reports no new issues, denies abdominal/flank pain, further catheter obstruction, fevers/chills. He states that his urine has been light pink in color, without clots, and significantly more clear than the prior 3 days. He has had intermittent episodes of blood in his urine in the past, but never causing obstruction. His catheter is managed at home with regular (q3wk) changes and no recent traumatic catheterizations.

    He denies any new back/bone pain or unintentional weight loss.

    PMH:

    • Prostate CA
    • HTN
    • DM
    • CKD
    • CAD

    PSH:

    • None

    FH:

    • Non-contributory

    SHx:

    • No current or previous t/e/d use
    • Lives with wife

    Meds:

    • lisinopril 20mg p.o. daily
    • glyburide/metformin 1.25/250mg p.o. b.i.d.
    • atorvastatin 20mg p.o. daily
    • ASA 81mg p.o. daily

    Allergies:

    • NKDA

    Physical Exam:

    VS: T 98.4 HR 64 RR 13 BP 136/94 O2 99% RA
    Gen: Well-appearing, pleasant man in no acute distress.
    Abd: +BS, soft, NT/ND, no suprapubic tenderness, no CVAT
    GU: Foley catheter in place draining clear-pink fluid to leg bag, no clots. No evidence of trauma to urethra, no visible skin lesions. Testes descended bilaterally, no inguinal lymphadenopathy.

    Assessment/Plan:

    85M hx CaP (2009) s/p radiation and androgen deprivation therapy with urethral strictures requiring chronic indwelling catheter presenting with macroscopic hematuria. Given patient’s history, radiation cystitis is a likely cause of his symptoms. However, given the long-standing catheter, other considerations include trauma and infection. Also, recurrence or new malignancy must be considered. Will obtain UA, UCx, and schedule patient for cystoscopy with bilateral retrograde pyelogram. Also, educated patient on how to irrigate catheter if needed and provided ED precautions should obstruction persist despite irrigation attempts. Patient’s last surveillance PSA undetectable, continue routine follow-up.

    Differential Diagnosis of Macroscopic Hematuria

    Differential Diagnosis of Macroscopic Hematuria

    Important Historical Elements:

    • Painless: suggests malignancy
    • Painful: suggests calculi/infection
    • Urinalysis: presence of dysmorphic RBC’s, RBC/WBC casts, proteinuria suggest intrinsic renal disease
    • Timing: early (distal urethra), throughout (upper urinary tract), terminal (bladder neck, prostatic)

    Guided Lecture

    EM Ed
    Watch “Gross Hematuria: Just a Bit of Kool-Aid” from EM Ed. In this lecture Dr. Basrai reviews the differential diagnosis and management of macroscopic hematuria in the emergency department.

    References:

    1. Hicks, D., & Li, C.-Y. (2007). Management of macroscopic haematuria in the emergency department. Emergency medicine journal : EMJ, 24(6), 385–390. doi:10.1136/emj.2006.042457
    2. Mazhari, R., & Kimmel, P. L. (2002). Hematuria: an algorithmic approach to finding the cause. Cleveland Clinic journal of medicine, 69(11), 870–872–4– 876.
    3. Howes DS, Bogner MP. Chapter 94. Urinary Tract Infections and Hematuria. In: Tintinalli JE, Stapczynski JS, Cline DM, Ma OJ, Cydulka RK, Meckler GD, eds.Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York: McGraw-Hill; 2011. http://www.accessmedicine.com/content.aspx?aID=6362340. Accessed June 14, 2013.
    4. Sutton, J. M. (1990). Evaluation of hematuria in adults. JAMA : the journal of the American Medical Association, 263(18), 2475–2480.

    Hyperbilirubinemia

    Gray's: Pancreas Anatomy

    CC:

    Yellow eyes

    HPI:

    51yo AA male with hx DM, HTN, sarcoidosis presents with yellowing of eyes and full-body itching x3wks. This was associated with dark urine and loose, light-brown stools. He denies N/V, abdominal pain, PO intolerance, F/C, recent travel, weight loss. He states that this has not occurred in the past, and he does not have any prior history of post-prandial abdominal pain.

    PMH:

    • DM
    • HTN
    • Sarcoidosis

     PSH:

    • None

    FH:

    • No GI malignancy

     SHx:

    • No tobacco or drug use, 10 years of 10 drinks/wk stopped 1yr ago

    Meds:

    • lisinopril 20mg p.o. daily
    • pioglitazone 15mg p.o. daily
    • sitagliptin 100mg p.o. daily
    • lansoprazole 15mg p.o. daily

    Allergies:

    • Vicodin (rash)

    Physical Exam:

    VS: T 97.9 HR 102 RR 12 BP 128/68 O2 99% RA
    Gen: WA, NAD
    HEENT: Marked scleral icterus, PERRL, yellowing of posterior oropharynx and floor of mouth, MMM, no cervical lymphadenopathy
    CV: RRR, S1/S2 normal, no murmurs
    Lungs: CTAB with good air movement
    Abd: Obese, +BS, soft, NT/ND, no rebound/guarding, no palpable organomegaly, negative Murphy
    GU: No inguinal lymphadenopathy
    Ext: Warm, well-perfused, no LE edema, peripheral pulses 2+
    Skin: No visible skin lesions
    Neuro: AAOx3

    Labs:

    • CBC: 16/12.4/35.1/281
    • LFT: AST 281, ALT 302, AP 264, T.bili 22.1, D.bili 16.8

    Studies:

    • RUQ US: Biliary sludge, no stones, no GBW thickening, no pericholycystic fluid
    • ERCP: 3cm stricture of distal CBD, biopsies taken

    Assessment/Plan:

    51AAM w/DM, HTN, sarcoidosis with 3wks painless jaundice. Obstructive pattern along with only modest elevation of liver enzymes suggests the obstruction is likely extrahepatic which was supported by ERCP finding of a distal CBD stricture. Patient has no history of prior instrumentation to cause iatrogenic stricture, and while sarcoidosis is associated with cholestatic complications (portal granulomas), pathology from biopsy showed papillary adenocarcinoma. The patient was scheduled for surgery with a plan for initial laparoscopic survey of the abdomen followed by Whipple if no evidence of widespread disease.

    Imaging:

    ERCP

    ERCP

    3cm stricture of distal CBD

    MRCP

    MRCP

    Filling defect in the common bile duct with marked dilatation of the common duct and intrahepatic ducts.
    Findings may reflect an intraluminal mass or stone.

    CT Abdomen/Pelvis

    CT Abdomen/Pelvis

    Common bile duct stent present
    Expected air in the intrahepatic biliary tree and mild biliary ductal dilatation

    Differential Diagnosis of Hyperbilirubinemia: 1, 2

    A System for Hyperbilirubinemia

    Evaluation of Hyperbilirubinemia: 3

    Evaluation of Hyperbilirubinemia

    References:

    1. Heathcote, E. J. (2007). Diagnosis and Management of Cholestatic Liver Disease. Clinical Gastroenterology and Hepatology, 5(7), 776–782. doi:10.1016/j.cgh.2007.05.008
    2. Hirschfield, G. M., Heathcote, E. J., & Gershwin, M. E. (2010). Pathogenesis of cholestatic liver disease and therapeutic approaches. Gastroenterology, 139(5), 1481–1496. doi:10.1053/j.gastro.2010.09.004
    3. McGill, J. M., & Kwiatkowski, A. P. (1998). Cholestatic liver diseases in adults. The American Journal of Gastroenterology, 93(5), 684–691. doi:10.1111/j.1572-0241.1998.206_a.x