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.

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