Intern Report 7.12

Case Presentation by Derek Kennedy, MD

CC: Unobtainable

HPI: A 79-year-old woman who is nonverbal at baseline is brought to the ED via EMS for a decrease in responsiveness and increased work of breathing These symptoms were noted to begin this morning by nursing staff.  EMS reports an oxygen saturation of 96% obtained upon their nursing home arrival,  Pt minimally responsive to painful stimuli.

ROS, social and family history: Unable to obtain.

PMHx: Dementia, OA, psychiatric disorder. Per previous echo, pulm HTN noted. Per EMS, notes Pt recently diagnosed with heart failure but no EMR documentation found

PSHx: PEG tube

Medications: Zantac, neurontin, keppra, aspirin, aricept, actonel, namenda


Physical Exam:
Gen: Laying in bed, nonresponsive to verbal cues, responds to painful stimuli. GCS
Vitals: BP 144/92, HR 118, RR 19, T 37.6 obtained rectally, O2sat 100% on 4L NC
HEENT: Normocephalic, atraumatic, PERRLA, no tracking.  Dry mucous membranes with crusting at b/l commissure noted, edentulous at upper jaw, multiple broken teeth with enamel darkening noted along lower jaw.
Neck: No JVD
CV: RRR with no noted murmur, rub, gallop
PULM: Clear to auscultation b/l with coarse breath sounds throughout and expiratory wheeze noted at bases.
ABD: Soft, nontender, nondistended abdomen w/ bowel sounds
Fecal occult blood test positive, weakened rectal tone, gross light brown feces, no gross blood
MSK: FROM to passive pressure with pulses noted in all 4 extremities. No peripheral edema
Skin: Skin breakdown noted at the anterior neck, upper chest, Right forearm, Left thigh, perirectal region

Labs / Imaging / ED course

ABG: pH 7.35
pCO2 42
pO2 68
HCO3 23
O2sat 96.6

Na 151
Cl 115
Gluc 118

WBC 11.9
Hgb 10.4
Plt 202

INR 1.12
PT 12.0

Trop 0.318
Trop 4 hrs later 0.241

UA: Negative except 1+ prot, 1+ bact, unrecognized amorphous sediment.

Head CT no acute process, some chronic ischemic changes 2/2 microvascular disease and diffuse brain atrophy noted.




 Medical Course:
Pt responded well to 250cc 0.9%NS IVF bolus, eye tracking returned, repeat vitals BP 119/74, HR 114, RR 17, satting 96% on 4L NC.



1) Which of the following has been connected with elevated BNP in the absence of elevated troponin?

a) Subarachnoid hemorrhage
b) Acute kidney injury secondary to dehydration
c) Acute pulmonary embolism
d) COPD exacerbation
e) Anemia

2) Which of the following is an absolute contraindication for heparin use?
a) Elevated INR
b) Active GI bleeding
c) Chronic alcoholism
d) Hepatic disease
e) DIC without severe thrombocytopenia

3) Is elderly abuse a concern here?
a) No, with appropriate evidence in support
b) Yes, with appropriate evidence in support
c) Likely, without sufficient evidence of support
d) Likely no, without sufficient evidence of support


Answers & Discussion:

Questions 1: E. Troponin I is a commonly ordered lab in the ED. One study examining 69,299 patients admitted through the emergency department found 48% had their troponin measured. Of these, 2,344 patients (3.3% overall, or 7.0% of those that had a troponin I measured) had an elevated concentration. Of those with a positive troponin, 42.7% did not have ACS (3). Common causes of non-ACS troponin elevation in acutely ill patients include severe hypertension or hypotension, upper gastrointestinal bleeding,and sepsis (with or without acute respiratory distress syndrome).  Many chronic conditions also cause troponin elevation, including LVH, heart failure, pulmonary HTN, and kidney diseases, even when CKD is asymptomatic.  Musculoskeletal injury including rhabdomyolisis, blunt force trauma, and recent surgical intervention also have been identified.  Dehydration and resultant AKI (choice B), PE (choice C), and COPD exacerbation  (choice D) have also been connected to elevated troponins. SAH (choice A)  is less studied in the sense of direct troponin elevation, but a study evaluating nontraumatic SAH and troponins levels impacting hospital mortality shows the strong linkage(2).  Anemia does not cause elevated troponins, but has been connected to elevated BNP in patients already with diagnosed heart failure (1).   Major takeaway from this discussion is to not disregard non-ACS troponin elevation as an elevated troponin in the absence of ACS is most often associated with a worse prognosis to overall morbidity and mortality.  A table of common causes of troponin I elevation separated by system is provided below.

System Causes of Troponin Elevation
Cardiovascular Acute aortic dissection
Medical ICU patients
Heart failure
Apical ballooning syndrome
Cardiac inflammation
• Endocarditis, myocarditis, pericarditis
Infiltrative disease
• Amyloidosis, sarcoidosis, hemochromatosis, scleroderm
Left ventricular hypertrophy
Myocardial Injury Blunt chest trauma
Cardiac surgeries
Cardiac procedures
• Ablation, cardioversion, percutaneous intervention
Hypersensitivity drug reactions
Respiratory Acute PE
Infectious/Immune Sepsis/SIRS
Viral illness
Thrombotic thrombocytopenic purpura
Gastrointestinal Severe GI bleeding
Nervous system Acute stroke
• Ischemic stroke
• Hemorrhagic stroke
Head trauma
Renal Chronic kidney disease
Endocrine Diabetes
Musculoskeletal Rhabdomyolysis
Integumentary Extensive skin burns
Inherited Neurofibromatosis
Duchenne muscular dystrophy
Klippel-feil syndrome
Others Endurance exercise
Environmental exposure
• Carbon monoxide, hydrogen sulfide


Question 2: B. Heparin exerts its anticoagulative effect by activating and accelerating the proteolytic activity of plasma cofactor antithrombin. Heparin binds to the lysine site on antithrombin, producing a conformational change at the arginine-reactive site that converts antithrombin from a slow, progressive thrombin (factor IIa) inhibitor to a rapid inhibitor of thrombin and factor Xa, thereby preventing thrombus propagation (4).  Heparin also binds to a number of different circulating plasma proteins (acute phase reactants), blood cells, and endothelial cells, which contributes to its differing anticoagulative effects in different patients. Therefore, close and frequent monitoring of the aPTT is necessary to ensure a safe therapeutic range

Heparin is commonly used in clinical practice as an early invasive strategy for most cases of confirmed NSTEMI, but AHA guidelines recommend early invasive strategy in those ACS patients with associated high-risk indicators with an ischemia-guided strategy for those patients without such factors.  These include recurrent angina or ischemia at rest or with low-level activity, despite intensive anti-ischemic therapy, elevated cardiac-specific troponin level (troponin I or T), new or presumably new ST-segment depression, recurrent angina or ischemia with symptoms of congestive heart failure, an S3 gallop, pulmonary edema, worsening rales, or new or worsening mitral regurgitation, high-risk findings on noninvasive stress testing, depressed left ventricular function (e.g., ejection fraction < 40% on noninvasive study), hemodynamic instability, sustained ventricular tachycardia, percutaneous coronary intervention within previous six months, previous coronary artery bypass grafting (5).  Elderly patients, when compared to their younger counterparts, show a greater absolute and relative benefit to early invasive therapy even despite their risk of associated bleeding.  In general, compared with standard therapy with aspirin, the use of heparin does not reduce mortality, the need for revascularization, major bleeding, thrombocytopenia, or recurrent angina. Heparin use does increase the incidence of minor bleeding.

There are contraindications to the use of heparin as it is associated with several risks including those listed above. Absolute contraindications to heparin include known hypersensitivity, past or present heparin-induced thrombocytopenia and active bleeding (choice B).  Elevated INR (choice A) is a contraindication that can be reversed via FFP (shorter) or Vit K administration. Hepatic disease (choice D) leading to coagulopathy contraindicates heparin admin as well as chronic alcoholism (choice C) leading to both chronic hematologic changes as well as hepatic disease contraindicating heparin administration.  DIC (choice E) is the only option listed that is not a contraindication, absolute or relative, to heparin administration with the noted NOT severe thrombocytopenia, which is a contraindication.

Question 3: A. Untreated skin breakdown noted on exam, minimal medical works sent with Pt favor possible abuse.  Pt with normal limits creatinine making dehydration supporting neglect less likely and call by nursing home to EMS placed on day of change in mental status favoring appropriate care, which is the more likely scenario based off of her presentation.

Elderly abuse is an underrecognized problem in our society, and with the increasing survival rate of our nation’s population, this issue warrants further investigation. A systematic review in 2008 found 6% of older people surveyed globally reported abuse with a range of 3-27% across cultures. Psychological abuse was reported by nearly ¼ of those victims. US data from 2002 indicate that 1.6 million people live in 17,000 licensed nursing homes with another 900,000 in similar facilities.  When one takes into account the suspected rates of undiagnosed dementia, recurrent AMS in the elderly due to infectious and comorbid conditions, and the 41% of community-residing Medicare beneficiaries over 65 with difficulty with ADL’s, it is likely the 6% is an underreported sampling.  Physical, psychological, and sexual are the most reported insults, but several exist, including:

  • Physical Abuse—inflicting physical pain or injury on a senior, e.g. slapping, bruising, or restraining by physical or chemical means.
  • Sexual Abuse—non-consensual sexual contact of any kind.
  • Neglect—the failure by those responsible to provide food, shelter, health care, or protection for a vulnerable elder.
  • Exploitation—the illegal taking, misuse, or concealment of funds, property, or assets of a senior for someone else’s benefit.
  • Emotional Abuse—inflicting mental pain, anguish, or distress on an elder person through verbal or nonverbal acts, e.g. humiliating, intimidating, or threatening.
  • Abandonment—desertion of a vulnerable elder by anyone who has assumed the responsibility for care or custody of that person.
  • Self-neglect—characterized as the failure of a person to perform essential, self-care tasks and that such failure threatens his/her own health or safety.

While one sign does not necessarily indicate abuse, some tell-tale signs that there could be a problem:

  • Bruises, pressure marks, broken bones, abrasions, and burns may be an indication of physical abuse, neglect, or mistreatment.
  • Unexplained withdrawal from normal activities, a sudden change in alertness, and unusual depression may be indicators of emotional abuse.
  • Bruises around the breasts or genital area can occur from sexual abuse.
  • Sudden changes in financial situations may be the result of exploitation.
  • Bedsores, unattended medical needs, poor hygiene, and unusual weight loss are indicators of possible neglect.
  • Behavior such as belittling, threats, and other uses of power and control by spouses are indicators of verbal or emotional abuse.
  • Strained or tense relationships, frequent arguments between the caregiver and elderly person are also signs.


(1) Ralli S, Horwich TB, Fonarow GC. Relationship between anemia, cardiac troponin I,  and B-type natriuretic peptide levels and mortality in patients with advanced heart failure. Am Heart J. 2005 Dec; 150 (6) : 1220-7.

(2) Gupte M, John S, Prabhakaran S, Lee VH. Troponin elevation in subarachnoid hemorrhage does not impact in-hospital mortality. Neurocrit Care. 2013 Jun; 18 (3):368-73

(3) Waxman, D.A., et al., A model for troponin I as a quantitative predictor of in-hospital mortality. J Am Coll Cardiol 2006. 48(9): p. 1755-62.

(4) Hirsh J, Warkentin TE, Shaughnessy SG, Anand SS, Halperin JL, Raschke R, et al. Heparin and low-molecular-weight heparin: mechanisms of action, pharmacokinetics, dosing, monitoring, efficacy, and safety. Chest 2001;119(1 Suppl): 64S-94S.

(5) STEPHEN D. WIVIOTT, M.D., and EUGENE BRAUNWALD, M.D., Thrombolysis in Myocardial Infarction Study Group, Brigham and Women’s Hospital, and Harvard Medical School, Boston, Massachusetts. Am Fam Physician. 2004 Aug 1;70(3):525-532.

Amit Kumar, MD and Christopher P. Cannon, MD. Acute Coronary Syndromes:Diagnosis and Management, Part 1. Mayo Clinic Proceedings 2009 October; 84(10):

Maan Jokhadar and Nanette K Wenger. Review of the treatment of acute coronary syndrome in the elderly patients. Clin Interv Aging, 2009; 4:435-444.

Uptodate: Elevated cardiac troponin concentration in the absence of an acutre coronary syndrome.


Uptodate: Elder mistreatment: Abuse, neglect, and financial exploitation.

Senior Report 7.6

Case Presentation by Dr. Meredith Hill-Ciesielski, MD

CHIEF COMPLAINT(S): “Not acting right”

HISTORY OF PRESENT ILLNESS: This is a 68-year-old male who was sent in for a change in mental status.  The patient’s daughter went to visit her father.  When she arrived to the house her mom said he was not responding appropriately.  The daughter tried to get the patient up off the couch to take him to the hospital but he was unable to get out of the chair. He was also noted to have slurred speech.  When he arrived in the emergency department, he was unable to provide any history and was made a medical code.


Could not be obtained secondary to patient’s condition

PMH: Hypertension; otherwise unknown
Surg HX: Unknown
Medications: Maxzide 25 mg/37.5 mg, losartan 100 mg, other medications unsure
Allergies: The daughter believes he is not allergic to any medications
Social Hx: No drug use per family

PMD: He has a doctor but the daughter does not know his/her name

Vitals: Temperature was 36.3 C, HR 74 bpm, RR 12/m, blood pressure 166/86 mmHg, SpO2 100% on room air.  Weight 100kg
Capillary blood glucose:125 mg/dL
General: Patient’s eyes closed half way, moaned as he was transferred over to the stretcher.  No acute respiratory distress noted.
HEENT: pupils were pin point, not reactive to light. No pallor, mucous membranes moist. Patient had a weak gag on arrival
Neck: Supple, no rigidity
Resp: Normal respiratory effort with a slightly slow respiratory rate, clear on inspiration and expiration
Heart: Regular rate and rhythm, and no murmur or gallop. Pulses were intact and symmetrical
Abdomen: Soft, nontender, nondistended
Musculoskeletal: Distal pulses decreased but present. There is no clubbing or cyanosis
Skin: No rashes
Neurological: Patient was very sleepy, his eyes were closed but he would open to verbal stimuli. He would follow simple commands such as squeezing fingers.  He was able to lift arms off bed against gravity but had generalized weakness. His tongue protruded midline. Speech was unintelligible. Strength was 4/5 grip strength bilaterally. He could lift both legs and arms off the table but only for about one to 2 seconds; not sustainable.  He had no clonus.  He was very sleepy but when stimulated, he would attempt to try to follow commands


1. After placing the patient on a cardiac monitor, establishing IV access and obtaining a normal cbg (which was all done for patient) what would be your next step of action?

  1. Administer 0.2mg naloxne to patient
  2. Obtain blood cultures and give Ceftriaxone, Vancomycin and Acycolvir
  3. Send the patient for a CT head without contrast
  4. Adminsiter 500mg IM thiamine and send the patient to TCU for sobriety

2. While you are evaluating the patient you note that his respirations become more shallow and he is no longer responsive to pain nor verbal stimuli.  His head rolls back on the stretcher and his eyes close.  What is next step of action?

  1. Naloxone 0.2mg IV
  2. Shake the patient harder because he just may have overdosed on his clonidine
  3. Intubate the patient using RSI
  4. Send the Patient for a CT head without contrast

3. Assuming this patient does have a stroke syndrome, what/where is the most likely etiology?

  1. Basilar artery occlusion
  2. Dolichoectasia of the Vertebral artery
  3. Posterior inferior cerebellar artery (PICA) occlusion
  4. Posterior cerebral artery occlusion (PCA)

4. Patient returns from CT which does not show any acute intracranial hemorrhage.  His neurological status and exam is unchanged. You have consulted neurology and they feel the patient is a good tPa candidate.  What is your next course of action?

  1. Do not give tPa because the patient’s blood pressure is too high.
  2. Give the patient 9mg dose of tPa then infuse 80mg over the next hour
  3. Give the patient 90mg bolus of tPa then repeat the CT head
  4. Do not give tPa because the patient is too old.
  5. Do not give tPa because the patient is not having a stroke


Answers & Discussion:

Question 1 answers: 3, 1 (either one of these counted as the correct answer)

This patient’s exam and history are consistent with a possible stroke so obtaining a CT head would be a priority however, given that he was rather sedated and had pin point pupils, trying a small dose of naloxone prior to CT would not be a bad decision (naloxone is really only given to help with respiratory effort rather than wake them up, per se).  In a situation where the patient appears to have an acute onset of weakness and altered mental status with hard neurological abnormalities on exam, assuming alcohol intoxication would be disastrous. Working up and treating for meningitis is a consideration; however, there are few signs and symptoms on history and examination that would point you primarily to this disease process. The current American Heart Association and American Stroke Association recommend that a protocol be in place to expedite noncontrast CT scans for any potential stroke cases and have Pt/INR/aPTT drawn upon arrival so that treatment goals can be decided within 60 minutes.  The goal at our institution is 45 minutes from door to PT/INR/aPTT and 15 minutes from door to CT scan so that time can be allowed for lab processing and reading the CT as well as evaluation by the stroke team. CT head without contrast is the preferred first image modality because you are ruling out hemorrhage, tumor, abscess and stroke mimics.

Question 2 answer: 3

Ensuring an adequate airway is a must.  This patient lost the ability to protect his airway and should not be allowed to go to CT scan without being intubated.  Although not altogether inappropriate, a repeat dose of naloxone is unlikely to be of benefit after decompensating so quickly after the initial dose. Alternative diagnoses should be considered.  Clonidine can present in a similar manner to opioids; regardless, you would still want to protect the airway.

Question 3 answer: 1

This patient’s presentation is most consistent with a basilar artery occlusion. Typical findings of a basilar artery occlusion include: coma, quadrapeggia, and “Locked in Syndrome”. Locked in Syndrome Where the patient has complete paralysis with upward gaze.  Patient’s often present initially with unilateral weakness but may still show some weakness on the unaffected side.  Patients can have incoordination of limb movements and gait ataxia. You can see jerking or shaking often misdiagnosed as seizure. Patient’s can completely lose their ability to speak but will be able to open their mouths and stick out their tongue. Pooling secreation are a problem which is why airway management is critical here. Oculomotor symptoms are common so expect eye deviation or small pupils, ie this patient had pin point pupils.  Sensory deficits are usually not as common. Altered level of consciousness is also common. These types of stroke have higher mortality and poorer outcomes.

Dolichoestasia is elogation, widening and tortuosity of the artery.  Usually affects the verebral and basilar arteries. Usually the artery has a large external diameter and a thisn arterial wall. As the artery stretches and become more tortuous, the flow decrases resulting in a stroke like syndrome. As the artery dilates it can compress surrounding structures and cause symptoms or the artery can rupture which would lead to a catastrophic outcome.  Basically this patient’s symptoms are more consistent with a basilar artery stroke then verebral. Vertebral artery occulsion would present with symptoms of vertigo, nausea, vomiting and unilateral Horner’s syndrome and less likely a sedated state. Which is why this answer is less likely.

Posterior inferior cerebellar artery occlusion can cause a headache usually at the occiput. Patients have vomiting, gait ataxia, truncal ataxia and limb incoordination.  Patient will have abnomal cerebellar testing.  If the infarction in limited to the vermis, patients can have vertigo and nystagmus. Patients will also feel they are being pulled to the ipsilateral side. Ipsilateral facial pain (CN V), vertigo (vestibular nucleus), headache, Horner syndrome (descending sympathetic tract), dysphagia and dysphonia (CN IX and X), and ipsilateral loss of pain and temperature (spinothalamic tract). Wallenberg Syndrome is a neurological condition caused by stroke in vertebral or PICA.  Symptoms include dysphagia, hoarse voice, dizziness, nausea and vomiting, nystagmus, and ataxia.

Posterior Cerebral Artery Infarction typically presents with patients having visual field deficits (contralateral homonymous hemianopsia) and most commonly a unilateral headache.  Light touch deficits, loss of ability to read without agraphia, memory loss, unilateral 3rd nerve palsy, and minimal motor function loss.


answe 3.2

Question 4 answer: 2

Recombinant Tissue Plasminogen Activator (rtPA) is currently a very hot topic. Regardless, having made the diagnosis of basilar artery occlusion and stroke, he does meet criteria for administration.

Indications for rtPa:

  • -Measurable diagnosis of acute ischemic stroke: use of NIHSS is recommended. Symptoms should not be clearing, minor, or isolated.  Caution advised for giving tPa to patients with severe stroke (NIHSS>22)
  • -Age greater than of equal to 18
  • -Time of onset of symptoms less than or equal to 3 hours.


  • -symptoms consistent with SAH
  • -seizure with postictal residual neurological impairments
  • -previous head trauma or stroke in last 3 months
  • -previous MI in last 3 months
  • -previous GI or urinary tract hemorrhage in last 21 days
  • -major surgery within 14 days
  • -prior intracranial hemorrhage
  • -pretreatment systomlic BP>185 or diastolic>110 despite therapy given
  • -Evidence of active bleeding or acute fracture
  • -blood glucose<50
  • -INR>1.7
  • -use of heparin within preceding 48 hrs and a prolonged aPTT
  • -platelets count<100,000
  • -CT head shows multilobar infarction (hypodensity more than 1/3 cerebral hemisphere) hemorrhage or tumor
  • -failure of patient’s responsible party to understand risks, benefits, and alternatives to treatment with tPA after full discussion


Dosing of tPA:
The total dose of rtPA is 0.9mg/kg. With a max dose of 90mg. 10% given as a bolus then the rest given over 60 minutes. BP and neuro checks should be preformed every 15 minutes during for the first 2 hours after starting the infusion.

This patient did receive rtPA and then went for a confirmatory CT angiogram which was suspicious for a basilar artery thrombus. A confirmatory angiogram demonstrated diffuse atherosclerotic disease and critical stenosis of the basilar artery. His neurological examination improved remarkably and he was able to walk and talk upon discharge to home.  He elected to do physical therapy as an outpatient.


Caplan, et al. Posterior Circulation Cerebrovascular Syndromes. Oct 6 2013. Up to Date

Tintinalli’s Emergency Medicine 3rd ed.

Intern Report 7.11

Case Presentation by Dr.Kevin Belen, MD

CC: “My left arm hurts.”

 HPI: 39-year-old male presents to the emergency department complaining of left arm pain. The patient has a history of intravenous drug use and “skin popped” in the left upper arm earlier this week. The patient first noticed some mild pain and redness at his left shoulder 4 days ago that has slowly been spreading. He had ignored it until 2 days ago when he developed a fever and nausea, with pain that worsened with arm movement. The patient presented to the emergency department today because he is unable to move his left arm without excruciating pain and foul-smelling fluid began to drain from his arm this morning.

Constitutional: Subjective fever and chills
ENT: No sore throat
Respiratory: No SOB
Cardiovascular: No chest pain
GI: Nausea, no vomiting
GU: No hematuria
Musculoskeletal: Pain with movement at left shoulder/upper arm
Skin: Redness, foul smelling fluid from wound at left shoulder/upper arm
Neuro: No weakness, numbness or tingling
Psych: No depression

PMH: Hx of IVDA, multiple abscess I&D in emergency department, denied HTN, HIV or DM
Meds: None
Allergies: NKDA
Social: Homeless, +Tobacco, ½ pint of vodka per day, active drug use via IV and “skin popping”

Physical Exam:
Vitals: BP 156/98 Pulse 110 RR 16 Temp 39.2 oral Pulse ox 100% room air
Constitutional:  Thin male, Moderate distress apparent with movement of left arm, slightly diaphoretic
HEENT: No conjunctival pallor, sclera anicteric, oropharynx is dry
Respiratory: Clear to auscultation bilaterally
Cardiovascular: Tachycardic rate & regular rhythm, S1, S2, no murmurs or gallops.  +2 bilateral radial pulses.
Abdomen: Soft, no abdominal tenderness
Back: No spinal, paraspinal muscle, or CVA tenderness
Musculoskeletal: Significant tenderness with passive and active ROM at left shoulder.  Tender to palpation along the left clavicle, shoulder joint, and proximal half of humerus.  Strength at this joint unable to be assessed secondary to pain. Full strength and ROM throughout  right upper and bilateral lower extremities.  +2 edema about left shoulder joint.
Skin: Remarkable for erythema at the left shoulder from mid clavicle to mid humerus, tender to palpation through area of erythema, small black eschar approximately 2 cm in diameter overlying the lateral deltoid muscle where patient states he skin popped, foul-smelling thin gray fluid.
Neurologic: Awake, alert & oriented x3, sensation intact grossly through the bilateral upper and lower extremities.

Emergency Department Course:

Following the physical examination a focused bedside soft tissue ultrasound examination was performed yielding the following two images.


Figure 1.

Figure 2.


1. What is the most appropriate interpretation of the ultrasound findings?
A. Cobble-stoning appearance and subcutaneous abscess
B. Linear hyperechogenicity consistent with foreign body
C. Anechoic areas representing perifascial fluid and hyperechoic areas representing emphysema
D. Inadequate and patient should undergo an MRI

2. How would you best treat this patient?
A. Discharge with oral Trimethoprim and Sulfamethoxazole (Bactrim) and Cephalexin (Keflex)
B. Perform beside abscess I&D and follow up with PCP
C. Perform joint aspiration and admit to Medicine for IV abx
D. Consult Surgery for emergent debridement
E. Consult Surgery to remove retained needle tip and I&D abcess

3. In a bacterial culture, what would be the most common single isolate for this condition?
A. Staphylococcus aureus
B. Staphylococcus epidermidis
C. Group A streptococcus
D. Enterobaceteriaceae
E. Pseudomonas

Answers & Discussion:

  1. C
  2. D
  3. C

This patient presents with a history, physical exam, and ultrasound findings consistent and suggestive of necrotizing fasciitis.  Necotizing fasciitis (NF) is an uncommon but potentially lethal soft-tissue infection with mortality rates ranging from 6 to 76%  and carries a high morbidity. NF results in progressive destruction of the muscle fascia and overlying subcutaneous fat.  The muscle tissue is frequently spared because of its generous blood supply.   The clinical picture is similar to cellulitis which makes diagnosis sometimes difficult, however patients with NF are often noted to have pain out of proportion to exam and thus a high clinical suspicion is required  as delay in diagnosis portends greater morbidity and mortality.  Infection typically spreads along the muscle fascia due to its relatively poor blood supply.  Initially, the overlying tissue can appear unaffected.  Patients initially present with tenderness, erythema and marked subcutaneous edema.  Further in the course signs of gangrene (bullae, eschars) may appear.  Crepitus may be present but is not a requirement for diagnosis, and is found in only 12–36% of patients .  Tissue destruction leading to thrombosis of small blood vessels and destruction of superficial nerves in the subcutaneous tissue will cause anesthesia in the involved area and may precede the appearance of skin necrosis. NF can have rapid progression and extensive destruction can occur, leading to systemic toxicity, limb loss, or death. Conditions associated with necrotizing soft tissue infection include diabetes, drug use, obesity, immunosuppression, recent surgery, and traumatic wounds  .

Necrotizing fasciitis is a synergistic bacterial infection usually due to mixed flora.  NF can be caused by gram-positive, gram-negative, aerobic, and anaerobic bacteria but, Group A streptococcus was the most common bacterial isolate.  There are two types of necrotizing fasciitis.  Type 1 is polymicrobial and involves non-group A streptococci plus anaerobes.  In type 2, the pathogen is group A beta-hemolytic streptococci and the infection is typically found in the extremities.  A substance in the cell wall of streptococci causes separation of the dermal connective tissue, resulting in continued inflammation and necrosis. Streptococcal necrotizing fasciitis is frequently associated with streptococcal toxic shock syndrome .

Radiographs may reveal gas in the tissues, but it is not a universal finding .  If gas is visualized in the tissue, type I necrotizing fasciitis or gas gangrene caused by clostridia  is most common.  However, plain films show subcutaneous emphysema when there is a moderate to large amount of gas within the tissues in only 17–57% of patients .

Ultrasound is not well studied in the diagnosis of NF but there are increasing case reports.  Ultrasound can offer a more rapid diagnosis than traditional imaging studies .  The findings which suggest NF include thickening of the deep fascia, diffuse thickening of the overlying fatty tissue, and a fluid layer of at least 4 mm in thickness along the deep fascia. Further study regarding performance characteristics in the use of ultrasound in the diagnosis is required.  Yen et al reported a sensitivity

of 88.2% and specificity of 93.3% for US in the diagnosis of NF using the aforementioned criteria.  Diagnosis is further supported by the findings of subcutaneous air, which is pathognomonic for NF.  Ultrasound can help distinguish NF from cellulitis.  Both conditions have edema and increased echogenicity of the subcutaneous tissue, however, fluid spaces tracking along the deep fascia strongly suggest the diagnosis of NF over cellulitis .

In the case study from which the images in the case report were obtained an 8- to 12-MHz linear-array probe was used.   The images above demonstrate increased echogenicity of the subcutaneous fatty tissue with interconnected thin anechoic spaces corresponding to perifascial fluid resulting in a cobblestone appearance. There was a gas layer just above the deep fascia which appears hyperechoic (Arrowheads) with posterior ‘‘dirty’’ acoustic shadowing in Figure 1.  In Figure 2, there was also subcutaneous emphysema (Arrow), but there was an adjacent area of subcutaneous fat that still appeared normal at that level (M)

Treatment of necrotizing fasciitis includes resuscitation, parenteral antibiotics against S. aureusStreptococcus, gram-negative organisms, and anaerobes as directed by Gram stain and culture findings and emergent surgical debridement,. The most important treatment is debridement, which is often extensive and often requires multiple washouts and debridements.  In the case of the DRH patient from which this report is based upon, the patient underwent emergent surgical debridement.  Sadly, I was foolish and did not save my ultrasound images which had similar but more impressive findings when compared to the images above.

Figure 1 shows  hyperechoic soft-tissue emphysema (arrowheads) with acoustic shadowing. The overlying subcutaneous fat (F) shows increased echogenicity with interlacing anechoic spaces (arrow) representing perifascial fluid spreading along the fascial planes (cobblestone appearance).


Figure 2 shows hyperechoic focus (arrows) with posterior acoustic shadowing above the deep fascia corresponding to gas bubbles.

1. Rosen’s Emergency Medicine, Concepts and Practices, 7th edition

2. Necrotizing fasciitis: early sonographic diagnosis. J Clin Ultrasound. 2011 May;39(4):236-9.

3. UpToDate: Necrotizing soft tissue infections

Intern Report 7.10

Case Presentation by Dr. Lauren Holmquist, MD

Chief Complaint: “I had chest palpitations”

History of Present Illness:
Patient is a 77-year-old female who presents to the Emergency Department after feeling heart palpitations earlier that day at home. She was made a medical code secondary to bradycardia and hypotension. In the resuscitation bay, patient states that she called the ambulance because her heart was racing.  History is somewhat limited due to underlying dementia. The patient has no complaints of dizziness, shortness of breath, chest pain, or abdominal pain. She denies any current chest palpitations.

According to the patient’s daughter, she had complained of feeling lightheaded earlier that day. She said that her mother had three episodes of dizziness and had fainted once while walking to the bathroom. After her fainting episode, EMS was called. The patient’s daughter denied tongue biting or loss of bladder or bowel continence.

Review of Systems:
Constitutional: Denies fevers or chills
Eyes: Denies vision loss
Ears, Nose, Mouth, Throat: Denies earache
Cardiovascular: Positive for history of heart palpitations
Respiratory: Denies cough or shortness of breath
Gastrointestinal: Denies epigastric pain, nausea, vomiting and diarrhea
Genitourinary: Denies dysuria
Musculoskeletal: Denies joint pain
Skin: Denies new rashes
Neurological: Positive for syncopal episode

Past Medical History: Hypertension, atrial fibrillation, diabetes, dementia, kidney disease (no dialysis), and cardiac stents in 1995 status most MI

Past Surgical History: Hysterectomy, cataract surgery

Medications:  Per the patient’s daughter, she takes lopressor 50 mg daily, cardizem 60 mg daily, simvastatin 40 mg daily, procardia 20 mg daily, digoxin 0.125 mg daily, isosorbide mononitrate 30 mg daily, potassium chloride 10 mEq daily, lasix 20 mg daily, seroquel 25 mg daily, aspirin 81 mg daily, clonazepam 0.5 mg daily, ativan 1 mg daily, oxybutynin 5 mg daily, donepezil

Allergies: Penicillin, codeine, shellfish

Social History: Patient denies any alcohol, tobacco, and illicit drug use

Family History: Hypertension

Physical Exam:
General: Patient is alert and oriented x 1 (to herself only). In no apparent distress. Non-toxic appearing. No slurred speech.
Vital signs: Blood pressure 92/40, pulse 57, respirations 16, temperature 36.7, pulse ox 96% on room air
Eyes: Pupils equal, round, and reactive to light. 3mm bilaterally. Extraocular movements intact
Ears, Nose, Throat: Dry mucus membranes
Neck: Supple, no lymphadenopathy, no JVD
Cardiovascular: Bradycardic, regular rhythm, S1 and S2 heard without murmurs. No pitting edema. Palpable and equal pulses in all four extremities.
Respiratory: Lungs clear to auscultation bilaterally. No wheezing or rhonchi heard.
Gastrointestinal: Soft, nondistended, nontender to palpation. No obvious palpable masses.
Musculoskeletal: Spontaneously moving all four extremities
Skin: Warm, dry
Neurologic: Alert and oriented. Speaking coherently. No facial asymmetry, tongue protrudes midline. No dysmetria or dysdiadochokinesia noted.  Muscle strength 4/5 in all four extremities. Sensation to light touch intact throughout entire face and all four extremities.

Labs/Imaging/ED course:

Accu-check: 266

Electrolytes: Na 135, K 5.8, Cl 103, CO2 22, BUN 29, Cr 1.72; Anion gap 10; Ca 9.1, Mg 2.0

CBC: WBC 9.8, Hb 11.2, Hct 36.3, Platelets 273

UA: Negative for infection

Troponin: 0.021

Digoxin level: 2.1

NT-Pro BNP: 5.077

Holm 1

Vent. Rate 42, QRS 82 ms, QT/QTc 458/382 ms
Holm 2

The patient was given a 500 cc fluid bolus.  She was also given insulin, D50 and sodium bicarbonate for treatment of hyperkalemia. A repeat set of vitals included a blood pressure of 83/42 and a heart rate of 42. The patient was transferred back to the module for further work up.


1) For this patient, what is the recommended initial treatment?
a. Calcium
b. Digibind
c. Hemodialysis
d. Transvenous pacing

2) Above what potassium level has been associated with 100% mortality in the untreated patient?
a. >5
b. >5.5
c. >6
d. >6.5

3) There are various other toxic ingestions that can present as hypotension and bradycardia. What is one physical exam finding that would distinguish clonidine overdose from the others?
a. Hyperglycemia
b. Lethargy
c. Miotic pupils
d. Visual disturbances


Answers and Discussion:
1) B
2) B
3) C

Question 1:
The patient in this case presentation is presenting with digoxin toxicity, which is manifested by hypotension, bradycardia, and elevated potassium levels.  This patient has a history of kidney disease and presents with an elevated creatinine; therefore her digoxin toxicity is most likely secondary to dehydration and renal failure, as the kidney eliminates digoxin. The treatment for digoxin poisoning is the administration of digoxin-specific fragment antigen-binding (Fab) antibodies (DigiFab). All other interventions are considered adjunctive. Digibind treatment should be reserved for cases of severe cardiovascular toxicity. In acute toxicity, antibody treatment should be used for a potassium value greater than 5 mEq/L or unstable dysrthmias.  Treatment of digibind is indicated in this patient because her potassium is 5.8 and she has symptomatic bradycardia.

Dose of Digibind (in number of vials): [Level x weight (kg)]/100  **round to nearest vial**

Due to the patient’s hyperkalemia and history of kidney disease, you may have been tempted to give calcium. While calcium administration is indicated in the setting of hyperkalemia to stabilize the cardiac membrane, the administration of calcium in the digoxin-poisoned patient may precipitate “stone heart”, also known as cardiac standstill. The theory of “stone heart” is actually quite controversial. While there is a fear that IV calcium can precipitate life-threatening arrhythmias in the digoxin-toxic patient, the study by Levine M et al concluded that calcium did not seem to cause cardiac standstill or increase mortality. The paper notes that there have only been five case reports of deaths in patients on cardiac glycosides after they had been treated with IV calcium. Digoxin inhibits the sodium-potassium ATPase pump, increasing intracellular sodium and calcium in the myocardium. Since calcium causes myocardial contraction, it is not illogical to believe that increased intracellular levels of the cation would produce irreversible contraction.

Hemodialysis is insufficient in digoxin toxicity because the drug has a large volume of distribution and is mostly protein bound, therefore, will not be removed with HD.

Pacing may be needed temporarily while waiting for Digibind to take effect. There have been reports of successful transcutaneous pacing, however it is generally recommended that transvenous pacing be withheld unless external pacing fails. Digoxin already irritates the myocardium, which may be worsened with the catheter in transvenous pacing.

Question 2:
Hyperkalemia develops in digoxin toxicity due to inhibition of the Na/K ATPase pump, and it is the most important predictor of outcome in the setting of acute digoxin toxicity. The serum potassium level is in fact a better predictor of mortality than the initial digoxin concentration. This was first shown in a classic study by Bismuth, C. before the advent of antidotal therapy using digoxin-specific antibody fragments. In this study of 91 patients primarily with acute digoxin toxicity rather than intentional overdose, nearly 50% of untreated patients with a potassium level between 5-5.5 died. No patients with a potassium level less than 5 died. 100% of patients (all 10 in the study) with potassium exceeding 5.5 died.

Even with Digibind, treatment of severe hyperkalemia with IV glucose, insulin, and sodium bicarbonate should be still done. All of these treatments were given in this particular patient.

Question 3:
Clonidine is a commonly used central alpha-2-adrenergic agonist, used in the management of hypertension. Stimulation of these receptors inhibits the release of peripheral catecholamines, which results in a decrease of heart rate, contractility, and peripheral vascular resistance. While a paradoxical hypertension may occur right after ingestion of clonidine, it ultimately manifest as hypotension and bradycardia, similar to digoxin toxicity. However, unlike digoxin, clonidine also stimulates the same mu receptor as opioids, leading to miotic pupils. This is not seen in digoxin overdose.

Both digoxin and clonidine overdose can cause lethargy. One of the characteristic features of digoxin toxicity is its visual disturbances, including yellow-green chromatopsia (also red, brown, and blue).  Beta-blocker and calcium channel blocker overdoses can also cause hypotension and bradycardia. Beta blocker overdose usually causes hypoglycemia while calcium channel blocker overdose can cause hyperglycemia.

Key Points:

  • Digoxin works by inhibiting the sodium/potassium ATPase pump on the cardiac cell membrane, which leads to increased intracellular calcium and extracellular potassium.
  • Hyperkalemia is biggest predictor of mortality in the acutely digoxin-toxic patient.
  • Digibind is sufficient for treatment of digoxin-induced hyperkalemia. For an exam, never give calcium to these patients, but note the theory of “stone heart” is controversial.
  • Common EKG findings: PVCs, Atrial fibrillation with AV dissociation, Atrial tachycardia with block, Nonparoxysmal junctional tachycardia, Bidirectional ventricular tachycardia
  • Treatment of choice is Digibind FAB. Atropine can be used for bradycardia with high AV block.
  • Chronic digoxin toxicity is often more difficult to diagnose, as symptom onset is more insidious. GI symptoms are less pronounced, whereas neurological manifestations may be more prominent. In chronic digoxin toxicity, hypokalemia is of greater concern.


  1. The Effects of Intravenous Calcium in Patients with Digoxin Toxicity. Levine, M et al. J Emergency Medicine 2011. Jan;40:41-6.
  2. Digitalis (cardiac glycoside) poisoning. Levine, M et al. UpToDate.
  3. Cardiac arrhythmias due to digoxin toxicity. Goldberger, A. UpToDate.
  4. Rosen’s Emergency Medicine, Concepts and Clinical Practice. 8th Edition.

VLS 1.6





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