Case Studies NUR 7202 One and Two

Case Studies NUR 7202 One and Two

Ashley Peczkowski

Wright State University

NUR 7202

CASE STUDIES NUR 7202 ONE AND TWO 21

Case Study One

1.  What are potential etiologies of this patient’s symptoms?

Differential diagnoses for the patient’s symptoms are thyroid storm, migraine, meningitis, and subarachnoid hemorrhage (SAH). The likelihood of diagnosis in order is as stated above with thyroid storm being the most likely to be the causative agent to SAH being the least likely cause. Each of the differential diagnoses need to be ruled in or out using information obtained from history, physical exam, and tests results prior to beginning treatment to ensure safe and effective therapy.

Thyroid storm also known as thyroid crisis or thyrotoxic storm is an increase in free fraction thyroxine (T4) and triiodothyronine (T3). This occurs in one of four ways: the thyroid is stimulated by trophic factors; there is activation of thyroid hormone synthesis and secretion causing release of excess hormone; store of preformed hormone are excessively released due to autoimmune, infectious, mechanical, or chemical cause; or exposure to extra-thyroid source of thyroid hormone from either endogenous source such as struma ovarii or thyroid cancer, or exogenous from factitious thyrotoxicosis (Bahn et al., 2011). Causes of this increase in thyroid hormones can come from a variety of diseases such as Grave’s disease, toxic multinodular goiter, subacute thyroiditis, or factitious thyrotoxicosis. If the patient has thyrotoxicosis (hyperthyroidism) and is not diagnosed, then thyroid crisis may occur from common medical events such as: anesthesia, stress, hypovolemia, pregnancy, labor, complicated deliveries, excessive palpation of the thyroid, infection, burns, ketoacidosis, and food poisoning from marine neurotoxin. The most common cause of thyroid crisis is from iodine increasing drugs. These drugs include: radioactive iodine therapy, propylthiouracil therapy withdrawal, lithium administration, stable iodine, iodinated contrast dyes, cytotoxic chemotherapy agents, aspirin overdose, organophosphate intoxication, and amiodarone (Klubo-Gwiezdzinska & Wartofsky, 2012). The patients’ most likely cause was her pre-existing Graves disease that was exacerbated by the administration of radioactive iodine (131I) therapy. Clinical signs include decompensated organ systems resulting in high fevers out of proportion to any infection as a result of ineffective auto thermoregulation from the hypothalamus or from increased basal metabolic rate with increased oxidation of lipids; tachycardia out of proportion to fever or dysrhythmias such as atrial fibrillation, supraventricular arrhythmias or ventricular arrhythmias without heart disease; congestive heart failure or reversible dilated cardiomyopathy. Gastrointestinal disturbances such as nausea, vomiting, and diarrhea from increased parasympathetic nervous system stimulation are common, as well as central nervous system excitability which can lead to agitation, confusion, emotional lability, paranoia, psychosis, status epileptics, stroke, coma, and basal ganglia infarction (Klubo-Gwiezdzinska & Wartofsky, 2012).

Thyroid crisis is a complex disease that can be hard to diagnosis. Diagnosis is not based on T3 levels since T3 levels can be normal and yet still have an increased T4 to T3 conversion. This process is called euthyroid sick syndrome and is seen in thyroid hormone binding protein disorders such as in pregnancy or with administration of drugs. Because of this, diagnosis is based more on signs and symptoms and there severity. Several semiquantitative scales have been designed to help practitioners’ diagnosis and treat thyroid crisis (Klubo-Gwiezdzinska & Wartofsky, 2012). For other endogenous causes of hyperthyroidism, the best blood test to obtain is a serum thyroid stimulating hormone (TSH) measurement. This measurement has the highest sensitivity (98%) and specificity (92%) for hyperthyroidism or hypothyroidism. Normal TSH is 0.3-5.5 mU/L and is called euthyroid. Hyperthyroid TSH levels are less than 0.3 mU/L and hypothyroidism TSH levels are greater than 5.6mU/L (Guidelines and Protocols Advisory Committee, 2010). The TSH test is further enhanced by evaluating the free T4 level and plotting the inverse log-linear relationship between the TSH and free T4. Apparent hyperthyroidism can have serum blood levels of elevated free T4 and T3 with TSH levels that are non-detectable; however, early hyperthyroidism may have normal serum T4 and free T4, elevated T3, and non-detectable TSH. The latter is considered T3-toxicosis. Lastly, sub-acute hyperthyroidism may show blood levels of normal serum free T4, normal T3 or free T3, and lower than normal TSH levels (Bahn et al., 2011). The TSH, T4 and T3 are regulated by the hypothalamic-pituitary-thyroid axis through a negative feedback loop (Guidelines and Protocols Advisory Committee, 2010).

One of the most obvious and notable physical signs of thyroid crisis are the cardiac manifestations which presents as tachycardia, arrhythmias, and cardiomyopathies that develop from high output states. This high output state results from a higher preload state from activation of the renin-angiotensin-aldosterone axis, with a combination of reduced afterload from the increased T4 relaxing effects on endovascular muscle cells. This dyssynchrony results in systolic hypertension with a widened pulse pressure. In combination with vomiting and diarrhea, volume depletion with hypotension and vascular collapse leading to shock can also occur. Further disruption from the high output state results in increased myocardial oxygen demands, myocardial infarction, and pulmonary hypertension. This excitability state that is induced also affects the hematological components of the body by causing leukocytosis with a shift to the left without the presence of infection. The inflammatory cascade is initiated and results in a hypercoagulability state. Associated factors from this include increased fibrinogen, factors VIII, factors IX, tissue plasminogen activator inhibitor one, von Willebrand factors, and an increased red blood cell mass. This hypercoagulability state leads to thrombosis formation which in turn can lead to pulmonary embolism and can either be the cause of or exacerbate the pulmonary hypertension. Other respiratory complications include respiratory failure from tachypnea from increased oxygen demands (Klubo-Gwiezdzinska & Wartofsky, 2012).

Besides nausea, vomiting and diarrhea, the patient may experience abdominal pain from delayed gastric emptying. The delay is caused by disruption in the neurohormonal regulation affecting the gastric myoelectrical activity. Hepatic damage can also occur from increased anaerobic metabolism and glycogenolysis which is used to create lactic acid. The increased lactic acid damages the hepatic cells leading to increased lactate dehydrogenase, aspartate aminotransferase, bilirubin, and alkaline phosphatase. The increased in alkaline phosphatase however is the result of increased osteoblastic activity in the bone and not hepatic damage. This results in increased serum calcium levels as well as a metabolic increase of ketones producing acidosis. Hyperglycemia is present in the beginning from the glycogenolysis and catecholamine-mediated insulin release blockade with increased renal clearance and body resistance. Once glycogen stores are depleted hypoglycemia occurs. Lastly renal dysfunctions occur from glomerulosclerosis and proteinuria from increased glomerular filtration rate; renal failure from rhabdomyolysis; urinary retention from detrusor and bladder dysfunction; and autoimmune complex-mediated nephritis (Klubo-Gwiezdzinska & Wartofsky, 2012). This patient is most likely to have thyroid crisis based on the history and physical findings of recent Grave hyperthyroidism diagnosis, chronic right upper quadrant pain, and a recent weight loss of 30 pounds.

Migraine is the second most likely diagnosis for this patient’s headache. Migraines are usually a hereditary disorder related to genetic predisposition (Silberstein & Dodick, 2013). There are two different theories on migraine development: one being cortical spreading depression (CSD) and the other brainstem generator. The theory of CSD is the main theory of thought behind migraines with auras. This is based on studies conducted on rats and pigeons where brain mapping was completed and then stimuli introduced with monitored response of the brains neural activity. The observation demonstrated that the aura before the migraine is the result of cortical neuronal activation immediately followed by postictal depression of the neuronal firing. The process is responsible for meningeal pain brought on by neurogenic inflammation, vasodilation, and manipulation of the blood brain barrier resulting in plasma protein extravasation. Manipulation of the blood brain barrier is obtained through activation of the brain matrix metalloproteinases which are responsible to opening the blood brain barrier to large molecule such as proteins (Estemalik & Tepper, 2013). The CSD wave of depression of neurons followed by a longer wave of inhibition runs at a rate of three to six mm/minute in multiple areas of the brain including the cerebellum, cortex, and hippocampus. This rate of speed is important because it is much slower than normal brain activity and causes large changes in ionic concentrations. This self-propagating wave of depolarization of the neuronal and glial cells is activated by potassium influx, glutamate influx, and sodium/potassium pump activation. This process helps neurologist understand which drugs can help prevent and stop an acute migraine attack. The unnecessary activation of these pumps is responsible for activation of central and peripheral trigemionvascular nociceptive pathways and thus pain outside of the meningeal irritation through vasodilation and neurogenic inflammation caused by release of inflammatory cytokines, neuroinflammatory peptides, and calcitonin gene-related peptide (Costa et al., 2013).

Non-aura migraines are more difficult to understand and therefore treat. This is based on the brainstem generator theory where there is a dysfunction in the brainstem nuclei that are responsible for central control of nociception. This dysfunction causes increased regional cerebral blood flow and activation of the trigeminal nerve. Others argue that this increase is the result of pain perception or increased activity of endogenous antinociceptive system. No matter what the cause of the increased cerebral blood flow, the dysfunction on the brainstem generator could either trigger a migraine or add to the central excitability of the trigeminal pathways (Pietrobon & Striessnig, 2003). Although this patient meets criteria for migraine and has a history of migraines, given the recent diagnosis of Grave hyperthyroidism and fever thyroid crisis is more likely.

The third most likely cause of the patient’s migraine is meningitis. Meningitis is mostly caused by either a bacterial infection (Streptococcus pneumoniae, Haemophilus, influenza type b, and Neisseria) or viral infection (Entrovirus). Despite the causative agent the immune system responds to the infection by attacking the organism in the subarachnoid space thus releasing cytokines and initiating the inflammatory cascade. The introduction of cytokines results in increased permeability of the blood brain barrier to allow leukocytes to enter for phagocytosis. This however, also allows large protein molecules to enter the meninges; creating interstitial edema. This in combination with cerebral vasculitis and systemic hypotension results in cellular hypoxia and death. The most common finding with meningitis is a severe headache, nuchal rigidity, sudden high fever, photophobia, phonophobia, confusion, and irritability. Common assessment tests include Brudzinski’s sign, Kernig’s sign, and nuchal rigidity. Brudzinski’s and Kernig’s sign both have a sensitivity of 5% with a likelihood ratio 0.97. Nuchal rigidity is more accurate with a sensitivity of 30% and a likelihood ration of 0/94. (Grandgirard et al., 2013; Mohseni & Wilde, 2012). This diagnosis is less likely based on the absent neck stiffness and transient fever.

Finally the diagnosis of subarachnoid hemorrhage (SAH) should be considered. This is the least likely cause because the symptoms of the patient do not directly fit the symptoms of SAH; however, because of its high mortality rate, SAH should be considered. A SAH results from a rupture in a thinned artery in the subarachnoid space. This thinning can be caused by smoking, hypertension, drug or alcohol abuse, lower BMI, first degree relative with SAH, or connective tissue disorders. At risk patients include older adults, women, or African Americans or Hispanics. This sudden rupture of an aneurysm causes a severe sudden headache commonly referred to as a thunder clap headache and meningeal irritation symptoms such as photophobia, blurred vision, nausea, vomiting, nuchal rigidity, confusion, or altered level of consciousness. A SAH is considered a medical emergency and needs immediate treatment (Rank, 2013). This diagnosis is the least likely based on the gradual onset, “hammering” pain, and absent neurological symptoms.

2.  Which of the following is not considered a diagnostic criterion of thyroid storm?

A.  Nausea and vomiting

B.  Tachycardia

C.  Tremor

D.  Fever

E.  Pulmonary edema

Of the listed symptoms tremors are the only one that is not on the diagnostic criteria list for thyroid storm. The diagnostic criteria for thyroid storm include degrees of elevated temperature; central nervous system effects such as agitation, psychosis, seizures, and coma; gastrointestinal upset such as nausea, vomiting, diarrhea, and jaundice; tachycardia, congestive heart failure symptoms, and atrial fibrillation with or without precipitating factors. These symptoms were discussed in detail previously. A point number is assigned to each of the following symptoms and there severity. After a thorough assessment is completed, the practitioner will add up the following points awarded to each category and severity. A score of 45 or greater is highly indicative of thyroid storm while a score between 25 and 44 suggests impending storm and a score less than 25 indicates that a thyroid storm is unlikely (see table 1). The chart was designed to help practitioners delineate between thyrotoxicosis, an abnormal amount of thyroid hormone concentration, and thyroid storm; which is the extreme state of thyrotoxicosis. There is no direct point at which thyrotoxicosis becomes a thyroid storm and treatment should begin early in thyrotoxicosis before the advancement of thyroid storm (Nayak & Burman, 2006).

The thyroid is responsible for setting the body’s metabolic rate and in thyroid storm this metabolic rate is drastically increased. The thyroid hormone also increases the density of beta-adrenergic receptors which enhance the effects of the catecholamines creating a stress response by the body. In the brain the thyroid hormone affects the myelination of the oligondendroglial cells and the myelin membrane. Excess thyroid hormones can cause demyelination and myelin membrane disruptions, inhibiting transmission. Along with affecting myelination these hormones are also responsible for increasing synaptic transmission, increasing the pain receptors, and increasing neurotransmitters such as serotonin and norepinephrine. The increase in synaptic transmission, pain receptors, and neurotransmitters, will in turn increase neuroelectrical activity. Because of these two seemly opposite effects, a person with thyroid storm can experience one extreme, such as coma, to the other, such as with seizures or psychosis. While fine hand tremors are a common finding in hyperthyroidism they are not a constant finding in thyroid storm and are therefore not considered part of the diagnostic criteria. More common signs included on the diagnostic criteria are the nausea, vomiting, tachycardia, fever, and pulmonary edema for reasons previously stated.