Senior Report 7.8

Case Presentation by Dr. Craig Sharkey, MD

HPI: 43 year old male brought in by EMS for altered mental status. History provided by EMS: Patient was at home, drinking alcohol. He was found by family at the bottom of the stoop. Family notes that although he was drinking, he did not appear intoxicated. He had been at his normal state of health prior to the incident. No further history can be obtained; family is on their way via private vehicle.

ROS: Unable to assess

PMHx: Unknown, per EMR: none
PSHx: Per EMR: none
Allergy: NKDA
Meds: unknown
Family History: Uncle died in 30s from heart attack
Social: + Alcohol

Physical Exam:
VS: T 36.5 BP 141/90 P 80 RR 18 SpO2 99% on 15 lpm via nonrebreather mask
General: Patient minimally responsive. Not warm to touch, nondiaphoretic. Gag intact, has spontaneous respirations.
Head: NCAT, no obvious external hematoma or abrasion
ENT: dried blood at nares, trachea midline, no JVD
Eyes: Pupils mid range, responsive to light, extraoccular movements unable to be assessed
CV: Regular rate and rhythm. No murmur/rub/gallop appreciated. 2+ radial and DP pulses appreciated.
Pulm: Clear to auscultation bilaterally. No wheeze/rhonchi/rales
GI: soft, nontender, nondistended. Bowel sounds appreciated.
MSK: No deformity
Neuro: Initial GCS 3. During initial exam, patient becomes arousable. He is able to say his name, but does not know the day/year/location. He would obey commands to move arms and legs, no gross focal deficit.

 

Labs:

Chem 7: 140/3.7/102/28/13/1.3/8.7

CBC: 7/13.1/193

UA: WNL

EtOH: 235

UDS: Neg

ECG
EKG 1

CXR
CXR

CT head/c-spine: Negative

On review of EMR, his last presentation was 9 years prior

ECG 2004
EKG 2

 

Questions: 

1) On repeat exam, he is still normotensive, no tachycardia. He has no current complaints of chest pain, dyspnea, dizziness, palpations, nausea. Given the patient’s presentation what is the most appropriate disposition:
a) Activate cardiac cath lab for suspected acute myocardial infarction, given his EKG changes.
b) Trend troponin, place in CDU for chest pain rule out and provocative testing for suspected underlying coronary artery disease.
c) Place in TCU pending sobriety and trend troponin.
d) Admit to cardiology on telemetry for sudden death prevention

2) While in the emergency department, he becomes unresponsive and the monitor is alarming. He is pulseless and the monitor is displaying a wide complex tachycardia. Your next action is:
a) defibrillation followed by 1.5 mg/kg lidocaine for V-tach prophylaxis
b) synchronized cardioversion followed by 1.5 mg/kg lidocaine for V-tach prophylaxis
c) synchronized cardioversion, admit patient for AICD placement
d) synchronized cardioversion, admit to MICU with toxicology consult

3) The pathology underlying his presentation is likely:
a) alcohol abuse, dehydration and electrolyte abnormality
b) membrane ion channel dysfunction
c) luminal defects in the coronary arterial circulation
d) undisclosed polysubstance abuse with adulterant

 

Filed under: Senior Report

Senior Report 7.7

Case Presentation by Dr. Adnan Sabic, MD

CC: I don’t feel well

HPI: Fifty seven year old female presents complaining of not feeling well since this morning. Patient complains of feeling dizzy, however denies feeling lightheaded. Patient denies passing out. She denies any chest pain, shortness of breath, nausea or vomiting. She does report few episodes of watery diarrhea early this morning. She does not have any other complaints.

PMH: HTN, HLD and ESRD on HD and was dialyzed 2 days ago and is due tomorrow

Examination:
Vital signs: BP 70/36, HR 32, RR 13, Temp 36.7, Pulse Ox 96% on room air
General: Patient is laying in bed, eyes closed, however easily arousable and answering questions appropriately
Eyes: PERRL, no conjunctival pallor
Neck: No JVD
Cardiac: Bradycardic, no murmurs appreciated
Respiratory: LCTAB
GI: Abdomen is soft, NT/ND
Msk: Fistula present in left upper extremity. No overlying redness.
Skin: Warm and dry
Neurological: Awake and moving all extremities spontaneously. No facial droop. Pupils are equal, round and reactive to light. Strength is 5/5 in upper and lower extremities bilaterally.

 

Following ECG was obtained:

adnan

Questions:

  1. Based on this patient’s presentation, what is the most likely to be her primary disorder?
    1. Hypocalcemia
    2. Hyperkalemia
    3. Hypemagnesemia
    4. Hypokalemia
  1. What is the best initial treatment for this patient?
    1. Calcium Gluconate 1 gm IVP
    2. NaHCO3 1 AMP IVP
    3. Atropine 0.5 mg IVP
    4. Albuterol 5 mg nebulized treatment
  1. What is the onset and duration of action of the drug that was administered in question 2?
    1. 1-5 minutes and lasts for 60 minutes
    2. 10-50 minutes and lasts for 6 hours
    3. 1 hour and lasts for 16 hours
    4. 2 hours and lasts for 24 hours

 

Answers & Discussion:

1)    2
2)    1
3)    1

Hyperkalemia is a very common presentation seen in the emergency departments across the country. Vast majority of the presentations are benign and most of the patients have no complications from it. However, hyperkalemia can be very serious and it can lead to death.

Hyperkalemia is defined as potassium greater than 5.5 mEq/L. Hyperkalemia is especially important in patients who are dialysis dependent. Usually ESRD patients are able to tolerate higher levels of potassium, however in patients who receive dialysis regularly, even potassium of 6.0 mEq/L can lead to severe presentations.

Most patients with hyperkalemia will be asymptomatic, however patients can present with generalized malaise, shortness of breath and in cardiac arrest. It is critical for ED physician to consider hyperkalemia in cardiac arrest in ESRD patients. In ESRD patients, it is imperative to obtain an ECG in any patient who presents with weakness, feeling short of breath, syncope or any other presentation that can be caused by hyperkalemia.

ECG changes associated with hyperkalemia have sequential progression. Patients with serum potassium levels of 5.5-6.5 mEq/L will usually have peaked tall T waves and shortened QT interval and possibly ST segment depression. Serum potassium level of 6.5-8.0 mEq/L will present with prolonged PR interval, decreased or disappearing P waves and widening of QRS. Levels higher than 8.0 mEq/L will have progressive QRS widening, bradycardia and absent P waves, which will lead to sine wave and eventuall ventricular fibrillation or asystole.

Patients who present with symptomatic hyperkalemia, should be evaluated in the resuscitation bay. IV access should be established as soon possible and patient should be placed on continuous cardiac monitoring. An ECG should be immediately obtained. If the ECG shows signs of hyperkalemia then treatment should be initiated immediately.

  • The first IV therapy should be calcium. Hyperkalemia causes irritation of cardiac membranes and this should be immediately treated with calcium gluconate or calcium chloride. Calcium gluconate can be administered thru the peripheral line. Calcium chloride should be administered thru central line. At least 1 gm of calcium gluconate or chrloride should be administered. Because of the short duration of action, definitive treatment should be initiated as soon as possible.
  • Insulin can be administered as well, which promotes intracellular movement of potassium. Five to 10 units of regular insulin should be administered.
  • Glucose should be supplemented too if the patient is euglycemic with D50.Frequent glucose checks should be ordered since insulin is metabolized by kidneys and in ESRD patients this can cause prolonged half life which can cause hypoglycemia.
  • Albuterol is an adjunctive treatment. It can be started while IV access is being established or during the process of obtaining the IV. Albuterol nebulized treatment, 5-10 mg. Albuterol shifts potassium into the cells which can last up to 2 hours.

HyperkalemiaTable

Hemodialysis is the definitive treatment for hyperkalemia and it should be initiated as soon as possible. Kayexalate can be administered as well, however according to some of the latest nephrology research, it should be the last resort. One of the most severe side effects of Kayexalate is gastrointestinal tract ulceration and/or necrosis which can lead to perforation and further complications.

Even though hyperkalemia is benign most of the time, ED physicians should be vigilant and on the lookout for it in ESRD patients. When symptomatic, aggressive measure should be taken and nephrology should be consulted immediately.


Filed under: Senior Report

Tox Time… Consult of the Week (COW)

COWj
Aimee Nefcy, MD
Fellow-in-training, Detroit PCC

 

The Bitter Truth

A 2 year old male was brought to the ER by family for decreased responsiveness. According to them, he was visiting Grandma’s house and had been seen in the back yard eating some red berries, a sample of which they have brought to the ER. He vomited once at home and then became rapidly lethargic. In the ER, he was initially unresponsive, then vomited twice and became agitated. He was bradycardic to 56 bpm and had a BP of 64/31. He was given atropine with improved vitals (117, 136/96). He was sedated, paralyzed, and intubated. Laboratory values were all within normal limits. In the ICU his BP was 90/45, HR 100. He was extubated after less than 12 hours. After extubation he had normal vital signs, but he remained drowsy yet agitated and confused. He had another episode of emesis, then improved. A photo of the plant was sent by the ER doc to the Toxicologist on call, and is shown here.

bitterj

 

1)    Ingestion of what type of plant should you worry about with a bradycardic, hypotensive, vomiting patient?

2)    What lab test available to the ER could be potentially helpful in diagnosing this?

3)    What tests are needed to determine the need for administration of a potential antidote?

4)    What is the plant shown here?

 

Answers:

1)    Digitalis-like plants, which commonly contain cardioactive steroids. The toxidrome for this extremely varied class of plants is identical for all: GI upset followed by bradycardia and cardiac dysrhythmias leading to cardiac arrest. Not all CAS’s are equipotent, however; eg, Convallaria majalis, Lily-of-the-valley, is relatively benign compared to Nerium oleander. Another consideration might be toxicity from organophosphate pesticides applied topically to the ingested plant, but sludge symptoms should be very prominent on exam.

2)    CAS’s in non-dig plants have some cross-reactivity with the digoxin assay, although the lab level does not correlate to the serum levels of the non-dig-CAS ingested. Children should have negative dig levels, and a detectable dig level is considered diagnostic of ingestion of a CAS.

3)    Additional labs needed to judge the severity of CAS toxicity include a potassium level (K>5 50% mortality, K>5.5 100% mortality without DSFab) and an EKG to evaluate for arrhythmias. Any of these, with or without symptomatic bradycardia, should prompt treatment with DSFab. DSFab has a limited ability to bind non-dig-CAS, therefore much larger doses are needed to treat a suspicious plant ingestion. Typically, 20-30 vials are needed depending on the severity of toxicity (compared to chronic digoxin needing 1-4 vials, and acute digoxin needing <10). Any CAS plant ingestion without GI symptoms, hyperkalemia, or EKG changes after 6hrs of observation in the ED can be cleared medically.

4)    Solanum dulcamara, known as woody or climbing nightshade, or bittersweet. This is a very common plant in Michigan, and is seen ubiquitously. The berries look and smell like little tomatoes and are seen in late summer to autumn. Solanine is the primary toxin, which has been shown in vitro to have acetylcholinesterase inhibition; there have been no reports of cholinergic toxicity, however. The primary toxicity is GI upset without CNS effects. The parts of the plant that are toxic are the leaves, fruits, stems, and shoots. This is in contrast to deadly nightshade, Atropa belladonna, which causes an antimuscarinic toxidrome.

Outcome: His symptoms were not felt to be consistent with this plant, which primarily causes GI upset. His dig level was negative. This patient’s sister had a history of being on carbamazepine, and he had detectable levels in his serum (thus depriving Aimee of her first-ever solanine-toxicity-causing-cholinergic-symptoms case report – so disappointed!). Within 24hrs of presentation he was back to baseline and was discharged with no permanent sequelae.

Recall that carbamazepine is a tricyclic anticonvulsant, and like other TCAs it tends to cause an antimuscarinic toxidrome with additional sodium-channel blockade. It is not clear why this patient was so bradycardic on presentation; possible confounders include coingestions, or maybe hypoxia from a seizure or aspiration.


Filed under: Toxicology

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

NKDA

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
NEURO: AxOx0

Labs / Imaging / ED course

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

BMP:
Na 151
Cl 115
Gluc 118

CBC:
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.

PCXR:
Derekxrayj

 

ECG:
ecgj

 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.

 

Questions:

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
Arrhythmia
Medical ICU patients
Hypotension
Heart failure
Apical ballooning syndrome
Cardiac inflammation
• Endocarditis, myocarditis, pericarditis
Hypertension
Infiltrative disease
• Amyloidosis, sarcoidosis, hemochromatosis, scleroderm
Left ventricular hypertrophy
Myocardial Injury Blunt chest trauma
Cardiac surgeries
Cardiac procedures
• Ablation, cardioversion, percutaneous intervention
Chemotherapy
Hypersensitivity drug reactions
Envenomation
Respiratory Acute PE
ARDS
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
Hypothyroidism
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.

References

(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.


Filed under: Intern Report

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.

REVIEW OF SYSTEMS:

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

EXAMINATION OF ORGAN SYSTEMS/BODY AREAS:
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

Questions:

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)
Explanation:

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
Explanation:

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
Explanation:

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.

answr3.1

answe 3.2

Question 4 answer: 2
Explanation:

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.

Exclusion:

  • -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.

Sources:

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

Tintinalli’s Emergency Medicine 3rd ed.

http://www.csuchico.edu/~pmccaffrey//syllabi/CMSD%20320/362unit11.html

http://en.wikipedia.org/wiki/Anatomy_of_the_cerebellum


Filed under: Senior Report

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.

ROS:
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
PSH:None
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.

Figure1_initial

Figure 1.

Figure2_initial
Figure 2.

Questions:

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.
Figure1_final

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).

Figure2_final

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

References:
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


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