|
Case
Report -
A 20+ year-old Male with Fever, Tachycardia, and Altered
Mental Status
|
Sonalika
Khachikian , MD
A
20+ year old male in otherwise good health was brought to
the hospital after being “found down” at his
correctional facility. The patient was apparently found
unresponsive to verbal or tactile stimulus and was noted
to have evidence of vomitus and urinary incontinence by
the prison staff. He initially presented to an outside hospital
where he was noted to display some moaning, thrashing, screaming,
and combative behavior at times; the patient was given Haldol,
Benadryl, and Ativan to control his behavior. At the outside
hospital he was noted to have a rectal temperature as high
as 105.6, a head CT scan was reported as negative, and obtained
cerebrospinal fluid (CSF) was without signs of infection.
The patient was transferred to Albany Medical Center for
further work-up. Upon arrival, the patient’s clinical
condition was without much change and he was still very
agitated. Incidentally, the ER staff found a 1cm piece of
paper in his stool.
Past
medical history is insignificant. Social history is positive
for remote drug abuse including marijuana and cocaine. Per
the prison medical records, he was not taking any medications.
Admission
vital signs were as follows: temperature of 102, BP 144/68,
pulse 158, respiratory rate 38, and oxygen saturation 98%
on 3L. The patient was in four point restraints, diaphoretic,
occasionally thrashing around on the stretcher. His skin
was warm and sweaty. His pupils were noted to be dilated
to 7mm, mucous membranes were moist, and there was an abrasion
on his tongue consistent with biting. There was no evidence
of jugular distension, lymphadenopathy, or nuchal rigidity
but his neck examination was significant for a slightly
enlarged palpable thyroid. Lungs were clear. Cardiac exam
revealed tachycardia but regular rhythm without murmurs.
Abdominal exam was within normal limits. Neurologic exam
was limited due to his altered mental status but did respond
to painful stimuli. Kernig’s and Brudzinski's signs
were negative. Peripheral pulses were 2+ throughout.
Various
lab studies were performed in order to ascertain this patient’s
diagnosis. The pertinent positive and negative lab findings
are included in the table below. All blood cultures drawn
were negative. Urine and serum toxicity screens were weakly
positive for benzodiazepines. An electrocardiogram revealed
sinus tachycardia at 154 beats per minute with no ischemic
changes noted. Chest X-ray (CXR) showed no active disease.
Table 1. Laboratory Data
| WBC
count |
2,400
/ mm3 |
| Hemoglobin |
13.2
gm/dL |
| Hematocrit
|
37.2% |
| Platelets |
92,000
/ uL (L) |
| Glucose |
87
mg/dL |
| Creatinine
Kinase |
3892
IU/L (H) |
| Troponin
I |
0.2
NG/mL |
| Alkaline
phosphatase |
141
IU/L (H) |
| AST |
87
IU/L (L) |
| ALT |
58
IU/L |
| Ammonia |
41
Umol/L |
| Thyroid
Stimulating Hormone (TSH) |
<0.01
UIU/mL (L) |
| Free
T4 |
5.42
ng/dL (H) |
| Triiodothyroxine
(T3) |
248
ng/dL (H) |
| Thyroid
stimulating Immunoglobulin |
281
ng/dL (H) |
| Thyroglobulin
Antibody |
227
U/mL (H) |
| Thyroid
Peroxidate autoantibody |
727
ng/dL (H) |
*Note:
(H) indicates high and (L) indicates low
DISCUSSION
When
this patient first presented, the initial differential diagnosis
included severe anxiety disorder, sepsis, neuroleptic malignant
syndrome, thyroid storm, drug toxicity including anticholinergic
or sympathomimetics (cocaine, PCP, amphetamines), hypertensive
encephalopathy, and meningitis (CNS infection).
A
few of these above differentials were eliminated rather
early – it was unlikely to be a severe anxiety disorder
because this would not account for his febrile state or
significantly altered mental status. Hypertensive encephalopathy
was also excluded from the list because he had no prior
history of hypertension, the patient’s blood pressure
was not dramatically increased, and he had no other evidence
of hypertensive changes--retinal hemorrhages, papilledema,
intracerebral or subarachnoid bleed.
Neuroleptic
malignant syndrome (NMS) is usually induced by a reaction
to antipsychotic medications (haldol being the most common),
where there is a central nervous system dopamine receptor
blockade. Common symptoms in NMS include severe hyperthermia,
extreme muscle rigidity, altered mental status, tremors,
labile blood pressure, and diaphoresis. If left untreated
death can occur. Since our patient was in no state to elicit
a complete history regarding ingestion of medications, dantrolene
was prophylactically administered to prevent death. Dantrolene
works by blocking the release of calcium from the sarcoplasmic
reticulum, thus decreasing the hypermetabolic state occurring
in the muscle leading to nonspecific muscle relaxation.
In this case dantrolene was not found to improve the patient’s
condition.
Once
laboratory data started returning, further potential etiologies
continued to be ruled out. Infectious meningitis was deemed
unlikely after the patient had two negative lumbar punctures
(CSF revealed normal glucose, normal protein, and no white
blood cells). Sepsis was no longer believed to be the etiology
of the patient’s condition given the leukopenia, negative
CXR and negative blood cultures. Drug induced toxicity was
also deemed unlikely given the unremarkable urine and serum
toxicity screens. It should be noted that certain drugs
(for ex. Ecstasy) are not picked up on toxicity screens
and therefore the diagnosis of substance abuse toxicity
cannot be completely eliminated.
Finally,
given the patient’s clinical condition and suggestive
lab data of an extremely elevated free T4 and T3 in the
setting of a decreased TSH, the diagnosis was confirmed.
The elevated thyroid stimulating immunoglobulin indicated
that there was new hormone synthesis likely from Graves’
disease. Graves’ disease can also cause a transient
leukopenia and thrombocytopenia. Thyroid storm can cause
nonspecific abnormalities in the liver enzymes which usually
resolve after the acute crisis. On further probing it was
concluded that the patient had been suffering from hyperthyroidism
for years. Prior complaints included tremulousness, increased
appetite with a marked increase in oral food intake without
any significant weight gain. He also reported increased
frequency in bowel movements, diaphoresis, and palpitations.
HOSPITAL
COURSE
After
the diagnosis of thyroid storm was established, the patient’s
tachycardia was treated with propanolol, a beta-blocker.
Propanolol is most frequently used because it can be delivered
via intravenous route initially and has the potential to
be switched to oral or per tube. Hyperpyrexia was managed
with acetaminophen and a cooling blanket. It is important
to remember to avoid salicylates as they compete with T3
and T4 for binding of thyroid binding globulin and can therefore
increase the free hormone levels in the body. The patient
was also started on high dose intravenous steroids. Glucocorticoids
work by blocking peripheral conversion of T4 to T3, the
active form of thyroid hormone. They are also believed to
have a direct effect on the underlying autoimmune process
and have shown to improve outcome in some studies. The patient
also received methimazole, a thionamide, which prevents
new thyroid hormone synthesis. Once the patient’s
condition was more stable, he was evaluated for total thyroid
removal. With all factors considered, it was decided that
a total thyroidectomy would serve as the best treatment
option. The patient underwent surgery without any complications
and was started on thyroid hormone replacement post surgery.
THYROID
STORM
Thyroid
storm is a rare disorder with a prevalence of only 1-2%
usually amongst persons with hyperthyroidism. The disease
may occur at any age but usually affects women in the third
to sixth decade of life. It is commonly seen in the poor
or underserved populations because this group usually lacks
access to routine medical surveillance.
Thyroid
storm still remains a clinical diagnosis and therefore it
is of great importance to include the disease on the differential
of patients presenting with fever, tachycardia, and delirium.
Furthermore, clinicians should treat patients on clinical
suspicion alone and should not delay for thyroid function
tests to return. Laboratory values suggest the diagnosis
but cannot actually distinguish between hyperthyroidism
and thyroid storm. If left untreated the mortality rate
is as high as 75 to 90%.
Many
believe that thyroid storm is a serious complication of
untreated Grave’s disease but can also be associated
with toxic multinodular goiter. The elevation of thyroid
peroxidase antibody and the thyroglobulin antibody helped
the medical team to identify untreated Graves as the etiology
of this thyroid storm. However, thyroid storm can be precipitated
by several different triggers including infection, trauma,
surgery, and diabetic ketoacidosis. These conditions precipitate
thyroid storm by the release of cytokines and acute immunologic
disturbances caused by the acute inciting factor.
Treatment
options are those as stated above with this patient. Fortunately,
post surgery, this patient reported feeling the best he
had in several years. He was discharged out of the hospital
on Synthroid in improved health.
REFERENCES
1.
Larsen. Special Aspects of Thyrotoxicosis.
In: Textbook of Endocrinology. 10th edition. Elsevier,
2003: 412-414.
2.
Mechem C. Severe hyperthermia: Heat strokes;
Neuroleptic malignant syndrome; and malignant hyperthermia.
Up to Date Online. 2004.
3.
Singhal A. Thyroid Storm. eMedicine.
2004.
4.
Connery LE, Coursin DB. Assessment and
therapy of selected endocrine disorders. Anesthesiology
Clinics of North America 2004;22: 526-528.
5.
Ross DS. Treatment of thyroid storm. Up
to Date Online. 2004.
6.
Manifold CA. Hyperthyroidism, Thyroid storm,
and Graves Disease. eMedicine. 2004.
7.
Weetman AC. Graves’ disease. N
Engl J Med. 2000 Oct 26;343(17):1236-48.
8.
Feldt-Rasmussen U. Serum thyroglobulin
and thyroglobulin antibodies in thyroid diseases. Pathogenic
and diagnostic aspects. Allergy 1983 Aug; 38(6):369-387.
9.
Berkenblit GV, Moore WT. Thyroid Disorders.
In: Cheng-Zaas (eds) The Osler Medical Handbook.
1st Edition. Johns Hopkins University, 2003: 387-397.
|
