Intern Report Case Discussion 1.4

intern-report

Presented by Devon Moore, MD

Chief Complaint:
She does not voice a specific chief complaint.  She was brought in as a medical code to ED by ambulance from home for “not acting herself”

History:
This is a 59-year-old woman brought into the emergency department as a medical code from home by ambulance.  According to family members, the patient appeared to be confused.  She does not seem to be acting herself, and she is very unsteady on her feet.  This occurred within the past couple of hours.  The patient is conscious but does not seem to be responding appropriately to family members.  On arrival the  patient is alert and oriented to person.  She is able to answer simple questions and follow simple commands.  She denies any complaints of a headache at this time.  No chest pain, difficulty in breathing, abdominal pain, nausea or vomiting.  She denies any extremity-related complaints.  She has had no recent illnesses.

Past Medical, Family, and Social History:
PCP:  The patient does not have a primary care physician.
PMH:  HTN.  It is negative for diabetes, known CAD or stroke.
SH:  Negative.
Meds:  She is not currently on any medications.
FH:  HTN, and negative for diabetes or CAD.
SOCIAL:   She lives with her daughter.  She does not smoke tobacco; consume alcohol or use illicit or I.V. drugs.

Physical Exam:
Vitals: BP was 225/130, HR was 94 and regular, and RR was 18.  Temperature was 36.5.  99% RA

General: She was conscious.  She was alert, but her speech was difficult to understand.  It appears that she may have had either an expressive aphasia, or possibly some mild dysarthria.  She was trying to tell me her name, but it was not understandable.  When asked to take a deep breath, she would open her mouth wide as if to take a deep breath, but she would not breathe deeply.  She did this repeatedly. HEENT: On exam, there was no trauma or abnormality of her scalp. The pupils were about 4mm, round and reactive to light.  EOM were intact; however, she had some element of a nystagmus (not clearly horizontal or vertical).  It may be rotary.  Her fundi looked to have a slight indistinctness of her left fundus and optic disc.  There was no obvious hemorrhage.  Her right optic disc was sharp without any obvious hemorrhage.  Her mouth was without intraoral lesions, and she had a positive gag reflex.  Her neck was supple with no nuchal rigidity.  No meningismus.  Trachea was midline without deviation.   Carotids were 2+ and without bruits.  No JVD.
RESPIRATORY: CTA bilaterally, with no rales or wheezes.  She was not cyanotic or diaphoretic.  No accessory muscle use.
CARDIAC: normal S1 and S2.  No S3 or S4 gallops.  No murmurs or rubs.  Good distal pulses.  Chest wall was non-tender.
ABDOMEN: negative.
MUSCULOSKELETAL: good pulses, no acutely inflamed joints.  Symmetric muscular strength and tone, and is able to move her extremities distally.
NEUROLOGIC: awake, alert and oriented to person.  No obvious sensory deficits to soft touch.  Deep tendon reflexes were hyper-reflexic.  Patella and Achilles were 3+.  She had clonus of both lower extremities and a slightly up-going toe on the left.  She had a downward plantar response on the right.  She had dysmetria seen with the left hand (right not tested).  Gait not tested, but when transferring her from EMS bed to resuscitation bed, she was uncoordinated and constantly fell on her left side while trying to “scoot” to the left to the next bed.

Labs:
•    Accu-check was 192

Diagnostic Studies:
•    12-lead-EKG showed normal sinus rhythm at 87 bpm, normal axis, no ventricular ectopy, normal PR, QRS, and QT intervals.   A voltage criterion for LVH is met.
•    Single-view CXR did not show any evidence of infiltrate, pneumothorax, or effusion.  There was no significant cardiomegaly.

Questions:

1.    Which of the following would be the next most appropriate steps to take to make a diagnosis?
a.)     CBC, lytes, BUN, cr, U/A, UDS and SDS
b.)     Aortic angiography
c.)     TSH
d.)     CT Head
e.)     Plasma metanephrine testing, MRI abdomen

2.    Which is the most appropriate in management of this patients’ blood pressure?
a.)     I.V. vasodilators and/or adrenergic antagonists for rapid reduction in BP to obtain a normal level  (<140/90)
b.)    Maintain SBP <160 mm Hg, and give oral nimodipine
c.)    Reduce mean arterial pressure (MAP) up to 20-25% over the first hour of treatment, use short acting and titratable agents I.V., with constant patient monitoring
d.)    I.V. Alpha-adrenergic antagonist therapy only to reduce BP
e.)    SBP <160, DBP <110, and I.V. magnesium sulfate

3.)  Which of the following is most closely associated with the term ‘hypertensive emergency’?
a.)  SBP >200, DBP >120
b.)  SBP >200, DBP >120 with pre-existing conditions (CHF, CAD, Renal insufficiency)
c.)  acute end-organ damage
d.)  longstanding, poorly controlled HTN
e.)  papilledema

Case Discussion

According to the Joint National Committee (JNC-7), the classification system for hypertension is the following:
•    Prehypertension – Systolic blood pressure (SBP) 120-139mmHG or diastolic blood pressure (DBP) 80-89 mmHG
•    Stage I hypertension – SBP 140-159mmHg or DBP 90-99mmHg
•    Stage II hypertension – SBP >160 mmHg or DBP >100 mmHg
•    Stage III hypertension – SBP ≥180mmHg or DBP ≥ 110 mmHg¹

This guide is an estimate used for the basis of a treatment guideline in those who are asymptomatic, and without evidence of organic pathology.  There are many other factors to look at based on co-existing conditions.  In general, those in stage I should be on 2 antihypertensive, and those in stage II should be on 2 antihypertensive medications.

When looking at our case, we had a woman over the age of 55 with a known history of HTN.  When I checked her blood pressure, it was 225/130.  This is enough to raise an eye-brow and realize that this is acutely too high.  But what was more alarming with her picture is that she portrayed evidence of an altered mental status.  Her family said that she was “acting different,” and we also witnessed this during our physical examination.

Transient Hypertension
This is seen with other conditions such as anxiety, alcohol-withdrawal syndromes, sudden cessation of medications, and some toxicologic substances².  Treat the underlying cause.

Acute Hypertensive episode
This is considered stage III hypertension without signs or symptoms of impending target-organ damage².  Controversy exists for treatment in this category.

Hypertensive Urgency
Many physicians will tell you that there is really no such thing as “hypertensive urgency” because it doesn’t have much utility in practice.  It represents a risk for imminent target-organ damage, but it is all relative.  This is especially true in our practice because many of our patients don’t have (or don’t utilize) primary care physicians for regular check-ups and control of conditions.  This means that someone who has high blood pressure could have had it for many years without knowing; and that is the danger (silent killer).  Hypertensive crises affect less than 1% of hypertensive adults in the United States.

Hypertensive Emergency
This term is most closely associated with target-organ, or acute end-organ damage.  It encompasses a spectrum of clinical presentations where uncontrolled BP’s lead to end-organ dysfunction.  These include the following:

Neurological

o    Hypertensive encephalopathy
o    Cerebral vascular accident/cerebral infarction
o    Subarachnoid hemorrhage
o    Intracranial hemorrhage

Cardiovascular

o    Myocardial ischemia/infarction
o    Acute left ventricular dysfunction
o    Acute pulmonary edema
o    Aortic dissection

Other

o    Acute renal failure/insufficiency
o    Retinopathy
o    Eclampsia
o    Microangiopathic hemolytic anemia³

When reviewing the above, it seems that our patient fits most with the picture of a hypertensive emergency.  Because of the cerebellar features that were consistent with our physical exam, our suspicions should be raised for a neurological problem.  The next best test for diagnosing purposes would be imaging, looking for any intracranial process such as stroke or hemorrhage.  CT head without contrast is a practical choice.

CT head without contrast was read as the following:

1.) Large area of hemorrhage in the posterior fossa, greater in the right cerebellar hemisphere compared to the left.  There is effacement of the fourth ventricle and the brainstem in this region.  2.) Chronic small vessel ischemic disease.  3.) Remote infarcts in the midbrain.

Laboratory results are still an important part of the presentation, because they can clue one in to other evidence of organ function, such as renal impairment.  They can clue one in to certain ingestions (sympathomimetics, cocaine).  And if the clinical picture fits, they can clue one in to other less common etiologies for elevated blood pressure (i.e. thyroid disease, pheochromocytoma).  But if you rely only on the labs, they may not be helpful at all.

Laboratory Results:
K+ hemolyzed >8.0; other lytes within normal limits.  Accu-check is 192.  CBC is normal with no sign of coagulopathy.  SDS and UDS are completely negative.  UA is negative for infection, or protein.

When discussing treatment options, it is important to stay aware that someone presenting in a state such as this may have a failure of their normal autoregulation.  Cerebral autoregulation is the ability of the cerebral vasculature to maintain a constant cerebral blood flow (CBF) across a wide range of perfusion pressures.  Patients with chronic hypertension can tolerate higher mean arterial pressures (MAP) before they have disruption of their autoregulation system. However, such patients also have increased cerebrovascular resistance and are more prone to cerebral ischemia when flow decreases, especially if blood pressure is decreased into normotensive ranges.  Rapid rises in blood pressure can cause hyperperfusion and increased CBF, which can lead to increased intracranial pressure and cerebral edema.   Because of this, certain antihypertensive treatments can exacerbate these problems.

The most practical agents to use in this setting are those that are more short acting, and titratable through the I.V. route.  The goal should be to lower the mean arterial pressure (MAP) by no more than 20-25% within the first hour.  Chronically hypertensive patients can develop symptoms of brain hypoperfusion if their blood pressure is lowered to what is defined as a normal level.  The “normal” level may be below the limits of an individual’s adjusted autoregulation (about 25% below a patient’s baseline MAP).

Sodium nitroprusside is the medication of choice, but nitroglycerin and labetalol are also successfully used.  In regards to question #2, choice b would be used for a subarachnoid hemorrhage (SAH), choice d would be used with acute cocaine precipitated HTN, and choice e involves the world of obstetrics and gynecology.

Answers:

1. D

2. C

3. C

Click Here for an excellent review

References

1.    Joint National Committee (JNC) on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure
2.    Emergency Medicine: a comprehensive study guide, Tintinalli.  Sixth edition
3.    Emedicine: Hypertension

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