Case Studies NUR 7202 One and Two - Yola



Case Studies NUR 7202 One and TwoAshley PeczkowskiWright State UniversityNUR 7202Case Study OneWhat 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. Which of the following is not considered a diagnostic criterion of thyroid storm? Nausea and vomitingTachycardia TremorFeverPulmonary edemaOf 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. Based on the patient’s symptoms and diagnostic studies, which of the following management strategies is not appropriate? Abaltion with 1311 (RAI)ThyroidectomyBeta-blocker and a thionamide Lugol solutionCorticosteroidsThyroidectomy, beta blockers, thionamide drugs, and Lugol solution are indicated in the treatment of thyroid storm. Ablation with the use of 131I is not indicated for the treatment of thyroid storm because this increases the amount of thyroid hormone synthesis, further increasing the severity of the thyroid storm. Ablation with 131I has been used for decades for the treatment of hyperthyroidism and is mostly well tolerated. The medication is only indicated for patients who have been given thionamide drugs before treatment and have obtained a euthyroid state. This is because in some cases administration of 131I alone while increase the amount of free T4 thus further worsening the thyroid storm. Those at greatest risk include patient who are extremely symptomatic, elderly, in atrial fibrillation, heart failure, have pulmonary hypertension, in renal failure, have an infection, suffered a trauma, have poorly controlled diabetes, or have cerebrovascular or pulmonary diseases. Treatment with ablation 131I is indicated if the patient has been pre-treated with a thionamide before and after administration and are otherwise healthy (Bahn et al., 2011). Treatment for thyroid storm is aimed at stopping thyroid hormone synthesis, release of stored hormone, prevention of T4 to T3 conversion, and controlling peripheral effects such as adrenergic symptoms and systemic decompensation. This is completed through administration of several drugs for a multimodal effect. Not only is it important to use multiple medications but also the order and timing of medications is crucial. It is important to start treatment with thionamide first before treating with iodine therapy to prevent increased thyroid hormone synthesis. Starting with a thionamide drug such as propylthiouracil or methimazole first causes inhibition of the thyroperoxidase-catalyzed coupling process. This prevents iodotyrosine residues from combining to create T3 and T4. Other important benefits of thionamides are that they prevent thyroid follicular cell function and growth; cause an immunosuppressive effect by decreasing antithyrotropin-receptors, intracellular adhesion molecule one, and soluble interleukin two; cause apoptosis of intrathyroidal lymphocytes and reduce HLA antigen expression. While methimazole is prescribed most because of its longer half-life and therefore reduced dosing frequency; propylthiouracil has the added benefit of inhibiting T4 to T3 conversion in the peripheries. These drugs are given as propylthiouracil 200-300mg oral every six hours or methimazole 20-25mg oral every six hours until stable and then can be given 80-100mg orally once to twice a day. Both of these drugs can also be given rectally if the patient is comatose or methimazole can be given intravenously. Important side effects are abnormal taste, pruritus, urticaria, fever, arthralgia, agranulocytosis, hepatotoxicity, and vasculitis (Nayak & Burman, 2006). According to the Ohio Board of Nursing an acute care nurse practitioner may prescribe these drugs without limitation (Ohio Board of Nursing, 2013). Once the anti-thyroid medications have inhibited new thyroid hormone synthesis the medical treatment is then focused on reducing thyroid secretion of stored hormone. Iodine or lithium is used to prevent proteolysis of colloids and secretion of T4 and T3 into the peripherals. Timing of administration is again very important. Iodine solution, called Lugol solution, should not be given within the first hour of thionamide administration because if the thyroid has not been adequately blocked then the iodine will increase thyroid hormone synthesis, hormone stores, and further increase thyrotoxicosis. When given correctly Lugol solution greatly decreases serum T4, reducing levels to normal in four to five days. If the patient is allergic to iodine then lithium can be substituted at 300mg orally every six hours. Lugol solution is given either orally or as a saturated solution of potassium iodine given at three to five drops every six hours (Klubo-Gwiezdzinska & Wartofsky, 2012). According to the Ohio Board of Nursing an acute care nurse practitioner may prescribe these drugs for thyrotoxicosis (Ohio Board of Nursing, 2013). Thyroid hormone suppression is not enough for treatment of thyroid storm because there remain large amounts of circulating hormone in the peripherals. Other treatments including plasmapheresis or therapeutic plasma exchange with albumin to increase bound thyroid hormone, are quick fixes for acute emergency but only have therapeutic effects for 24-28 hours (Klubo-Gwiezdzinska & Wartofsky, 2012). Controlling systemic effects of thyrotoxicosis is the main supportive treatment while waiting for systemic hormone levels to equalize. Cardiovascular effects of thyroid storm are controlled by the administration of beta-blockers. Propranolol 60mg to 120mg orally every four hours or parenterally at 0.5mg to one mg bolus over ten minutes and then one to three mg over ten minutes every few hours as needed is most commonly prescribed. Esmolol 50-100?g/kg/min is also indicated for treatment as an alternative for acute thyroid storm. Other beta-blockers used are atenolol, metoprolol, and nadolol. Because of the increase in metabolism and increased amount of cardiac beta-adrenergic receptors, larger doses are needed for beneficial effect. Propranolol as the added benefit of reducing T3 levels by up to 30%. Because atrial fibrillation is common in thyrotoxicosis anticoagulation is recommended based on stroke risk factors. Lower doses of warfarin are needed because of the increased metabolism of vitamin K-dependent clotting factors. Finally, glucocorticoids are indicated for treatment because they reduce the peripheral conversion of T4 to T3 and also used to treat adrenal insufficiency, which is commonly seen in thyroid storm (Nayak & Burman, 2006). According to the Ohio Board of Nursing beta blockers, warfarin, and glucocorticoids can all be prescribed by an acute care nurse practitioner (Ohio Board of Nursing, 2013). Lastly surgical treatments such as early thyroidectomy have been used with success greatly reducing the mortality rate (Klubo-Gwiezdzinska & Wartofsky, 2012). Case Study TwoWhat is the most appropriate next step in this patient’s diagnostic evaluation? Contrast-enhanced CT scan of the brainMagnetic resonance imaging (MRI) of the brainLumbar puncture (LP) with cerebrospinal fluid (CSF) analysisElectroencephalogramNo further diagnostic testingMeningitis should be suspected in all patients with altered mental status, fever, and neck stiffness. Because of the patient’s age and symptoms, it is appropriate to obtain a stat head non-contrast head cat scan (CT) for evaluation of an acute hemorrhagic stroke. It is also an important evaluation test to determine the patient’s risk of herniation during a lumbar puncture. Even if the CT is normal there is still a risk for herniation. Signs associated with increased risk of herniation include deteriorating level of consciousness, signs of brainstem involvement, and a recent seizure (Tunkel et al., 2004). Once this immediate evaluation has been completed, the next step is to perform a lumbar puncture to test for meningitis. A cerebral spinal fluid (CSF) culture is considered to be the gold standard for bacterial meningitis diagnosis. Other tests are needed to help confirm the diagnosis and also support antibiotic treatment. These tests include serum inflammatory marker, blood cultures, skin biopsy, and urine antigen. The purpose of the lumbar puncture is to test to CSF for signs of bacterial meningitis such as polymorphonuclear pleocytosis, hypoglycorrhachia, and raised CSF protein levels. This also helps tests for viral meningitis versus bacterial. Bacterial meningitis has glucose levels in the CSF of less than 1.9mmol per liter, CSF glucose to blood glucose ratio of 0.23, protein concentration greater than 2.2g per liter, and a leukocyte level more than 2,000 per mm3. However, if protein levels are less than 0.5g per liter and leukocytes less than 100 per mm3, bacterial meningitis can still be present. CSF cultures are used to grow the bacterial to levels that are then identifiable for treatment. Once the correct organism has been identified then the best treatment can be initiated. It is important to perform the lumbar puncture before empiric treatment with antibiotics is initiated because detection level before treatment in a large case series was 88-70% while post antibiotic treatment was at 66-62% (Brouwer, Tunkel, & Beek, 2010). The most common pathogens for bacterial meningitis in the adult population is the community acquired Steptococcus pneumoniae and Neisseria meningitidis. For these two main bacterial pathogens the sensitivity of a lumbar puncture for a CSF gram stain is 69-93% for S. pneumoniae and 30-89% for N. meingitidis. Because of this it is recommended that blood cultures, latex agglutination test, and PCR are also obtained. Blood cultures are used to detect the organisms if the CSF cultures are negative. The blood culture tests are 60-90% sensitivity for S. pneumoniae and 40-60% for N. meningitidis. Latex agglutination test is used when bacterial meningitis is suspected but CSF cultures are negative. This is performed by testing serum containing bacterial antibodies against capsular polysaccharides in the meningitis bacteria. This test is known to only take 15 minutes and has a sensitivity level of 78-100%. Lastly a PRC is performed to detect the presence of meningitis bacteria DNA in the CSF. The sensitivity of this test is 61-100% in S. pneumoniae and 88-94% for N. meningitidis (Brouwer et al., 2010). A Magnetic resonance imaging (MRI) of the brain is not indicated in this patient because of the altered mental status. Early treatment is needed in patients with altered mental status to reduce mortality rates. The longer the delay, the higher the mortality rate and waiting on an MRI can take hours to even days. A MRI is useful in early meningitis before the bacteria have replicated enough to show positive results in the blood and CFS. A MRI can see abnormal meningeal enhancement early in the process however once the patient has experienced altered mental status the inflammatory damage is great enough to be seen in regular testing (Kamra et al., 2004). A contrast-induced CT scan of the brain is used to monitor complications of meningitis and not for initial diagnosis. A contrast-induced CT scan can evaluate for hydrocephalus, subdural effusion, empyema, infarction, parenchymal abscess, or ventriculitis. This type of CT can be normal in a patient with bacterial meningitis and therefore should not be used for diagnosis. Lastly, an electroencephalogram can be used to detect abnormal brain waves seen in meningitis but cannot be used to diagnose (Hughes, Raghavan, Mordekar, Griffiths, & Connolly, 2010).Which of the following is this patient’s most likely diagnosis? Viral meningitisFungal meningitisBacterial meningitisMycobacterial meningitisNoninfectious meningeal irritation The most likely diagnosis of this patient is bacterial meningitis. There are five different types of meningitis including: bacterial, viral, parasitic, fungal, and non-infectious. Bacterial have become more uncommon with the use of vaccinations and include the two main types: S. pneumoniae and N. meningitidis. Viral infections have a lower mortality rate, are more common, and include mainly enterococcus but also syphilis. Fungal infections are rare unless the patient is immunocompromised with either: HIV, diabetes, transplant recipient, or other immunocompromising conditions. Parasitic infects are common in third world countries and should be considered only in the patient has recently travel to a third world country. Lastly, non-infectious meningitis is cause by a comorbidity, rather than an organism, such as lupus or types of brain surgery (CDC, 2013). The normal opening pressure of an adult should range from 60 to 250 mm H2O and therefore anything over 250 is considered to be intracranial hypertension. Intracranial hypertension is indicative of a pathological state including meningitis, intracranial hemorrhage, and tumors. If a lumbar puncture is performed, the practitioner should remove the CFS slowly and the pressure should be monitored. The lumbar puncture should be stopped once the pressure level is about 50% less than the original pressure. An elevated opening pressure is commonly seen in bacterial meningitis and not in viral meningitis. Next the color of the CSF should be analyzed. Clear CSF is normal but turbid CSF is the result of abnormal findings such as hemoglobin and leukocytes. Another term is called xanthochromia, in which the CFS is yellow, orange, or pink from breakdown of hemoglobin into oxyhemaglobin, methamoglobin, and bilirubin. This can be caused by a variety of conditions such as meningitis or subarachnoid hemorrhage. Lastly the contents of the CSF are examined to revile the number of leukocytes, red blood cells, protein level, and glucose level. This patient most likely has bacterial meningitis because her CSF count has the indications of bacterial meningitis. Bacterial meningitis typically has an elevated opening pressure, a leukocyte count higher than 1,000 per mm3, mild or marked elevation in protein levels, and a normal to decreased CFS glucose level to serum glucose level ration. This patient has all of the above and despite her CSF glucose being normal it is greatly decreased compared to her serum glucose level (Seehusen, Reeves, & Fomin, 2003). Based on the Gram stain, which of the following antibiotic regimens is most appropriate in this patient? Penicillin GCeftriaxoneCeftriaxone and VancomycinAmpicillin and cefotaximeCefepimeThis patient is above the age of 50 and has a history of diabetes she most likely suffers from Streptococcus pneumoniae meningitis. S. pneumoniae is most commonly seen in patients under the age of two, older than 50 years of age, or have co-morbidities such as: splenectomy, multiple myeloma, hypogammaglobulinemia, alcoholism, chronic liver or kidney disease, cancer, Wiskott-Aldrich syndrome, thalassemia, diabetes, basilar skull fracture, or cochlear implant with positioners. This diagnosis is further supported by the gram stain that showed Gram-positive cocci pairs, many polymorphonuclear leukocytes, and few mononuclear cells. In up to 60% of pneumococcal meningitis there is a distant source of infection such as pneumonia, otitis media, sinusitis or endocarditis in which a consulted otorhinolaryngologist is recommended. Pneumococcal meningitis is a life threatening disease that can cause a meningitis triad of high fevers, nuchal rigidity, and altered mental status in up to 60% of cases. This can also present with a high rate of abnormal brain dysfunction presenting in focal neurological abnormalities (40%), seizures (25%), and coma (one in five admissions) (Brouwer et al., 2010). Pneumococcal meningitis used to be treatable with penicillin but the overuse of antibiotics has caused many cases to become penicillin resistant pneumococcal meningitis. Because of this it is recommended to started empiric treatment, based on the gram stain, with Vancomycin and an expanded-spectrum cephalosporin like ceftriaxone. This is based on current antimicrobial susceptibility patterns and the assumption that the organism is antimicrobial resistant. This drug regimen should be continued until CSF cultures identify the organism, at which time the drug regimen should be changed based on the presenting organism. Treatment is recommended for ten to 14 days once pathogen has been isolated (Tunkel et al., 2004). According to the Ohio Board of Nursing an acute care nurse practitioner may prescribe both antibiotics (Ohio Board of Nursing, 2013). Complete the following table. Table 1Cerebrospinal Fluid Analysis in MeningitisMeasurementNormalBacterial MeningitisViral Meningitis Fungal Meningitis Parasitic Meningitis Opening Pressure (mmH20)70-180Markedly ElevatedUsually Normal to Slightly Elevated Variable; Moderately Elevated Normal to Slightly Elevated WBCs0-5 Lymphocytes≥1,000 per mm3 Polymorphic Neutrophils <100 per mm3 LymphocytesVariable; 100-1,000 per mm3 Lymphocytes Variable; 100-1,000 per mm3 LymphocytesGlucose (mg/dL)45-85Normal to DecreasedUsually Normal to DecreasedDecreased Normal Protein (mg/dL)15-45Mild to Marked Elevation Normal to Elevated Elevated Elevated Modified from: (1). Seehusen, D., Reeves, M., & Fomin, D. (2003). Cerebrospinal fluid analysis. American Family Physician, 68(6), 1103-1109. Retrieved from (2). McAuley. (2013). Cerebrospinal Fluid (CFS) analysis- meningitis. GlobalRPh: The Clinician’s Ultimate Reference. Retrieved from . (3). Hancock. (2005). Lab values and analysis. The Practitioner’s Pocket Pal. Miami: MedMaster. 5.???? Should this patient receive adjuvant therapy with dexamethasone? Dexamethasone is indicated for adjunctive treatment for pneumococcal meningitis to reduce inflammation as recommended by Infectious Disease Society of America, European Federation of Neurological Sciences and British Infection Society (Brouwer et al., 2010). Dexamethasone reduces pro-inflammatory cytokines, monocytes, dendritic cells, astroglial cells, neutrophils, reactive oxygen substances, leukocyte adherence, and increases anti-inflammatory cytokines. Neurological damage that occurs during meningitis is not the result from the pathogen but for from the inflammatory cascade induced by the pathogen. Dexamethasone decreases the amount of nitric oxide (NO) and tumor necrotizing factor alpha (TNF-α) produced from astroglial cells that have been stimulated by pneumococcal cell wall. This combined with endothelial cell reduction in TNF-α, inter-lukin-1 (IL-1), and mononuclear cell inhibition of S. pneumoniae-induced IkBk phosphorylation and degradation of the binding of NF-kB to DNA. This results in the reduction of the inflammatory cascade. Reduction in inflammation in the brain results in lower intracranial pressure, brain edema, altered cerebral blood flow, cerebral vasculitis, neuronal injury, and CSF pleocytosis (Mook-Kanamori, Geldhoff, Poll, & Beek, 2011). Dexamethasone in addition to antibiotics has shown to reduce hearing loss and other neurological sequelae however did not show any significant benefit in overall mortality rate. This drug is recommended by infectious disease to be ordered on all patients with suspected or proven pneumococcal meningitis and continued if the CSF stain shows gram-positive diplococci or if blood or CSF cultures produce S. pneumoniae. Dexamethasone is given at the recommended dose of 0.15mg/kg every six hours for two to four days intravenously with the first dose given right before or with the first dose of antibiotics (Tunkel et al., 2004). According to the Ohio Board of Nursing, acute care nurse practitioners have prescriptive authority to order dexamethasone (Ohio Board of Nursing, 2013). Controversies on giving dexamethasone include prohibiting Vancomycin therapy to penetrate into the CSF by reducing meningeal inflammation and also possibly causing hippocampus apoptosis without cognitive impairment which can also be caused by S. pneumoniae infections. Despite these concerns the benefits out way the risk and dexamethasone is recommended for all patients with confirmed for suspected pneumococcal meningitis even if the pathogen is suspected of being highly resistant to penicillin and cephalosporins (Mook-Kanamori, Geldhoff, Poll, & Beek, 2011; Tunkel et al., 2004). ReferencesBahn, J., Burch, H., Cooper, D., Garber, J., Greenlee, M., Klein, I., ... Stan, M. (2011). Hyperthyroidism and other causes of thyrotoxicosis: Management guidelines of the American Thyroid Association and American Association of Clinical Endocrinologist. Thyroid, 21(6), 593-647. and Protocols Advisory Committee. (2010). Thyroid function tests in the diagnosis and monitoring of adults. The Clinical Practice Guidelines. Retrieved from , M., Tunkel, A., & Beek, D. (2010). Epidemiology, diagnosis, and antimicrobial treatment of acute bacterial meningitis. Clinical Microbiology Reviews, 23(3), 467-492. for Disease Control and Prevention. (2013). Meningitis. National Center for Immunization and Respiratory Diseases. Retrieved from , C., Tozzi, A., Rainero, I., Maria, L., Calabresi, P., Ayata, C., & Sarchielli, P. (2013). Cortical spreading depression as a target for anti-migraine agents. The Journal of Headache and Pain, 14(62), 1-39. , E., & Tepper, S. (2013). Preventive treatment in migraine and the new US guidelines. Neuropsychiatric Disease and Treatment, 709-720. , D., Gaumann, R., Coulibaly, B., Dangy, J., Sie, A., Junghanss, T., ... Leib, S. (2013). The causative pathogen determines the inflammatory profile in cerebrospinal fluid and outcome in patients with bacterial meningitis. Mediators of Inflammation, 1-12. , J. (2005). Lab values and analysis. In The Practitioner’s Pocket Pal (2nd ed.) pp. 5-6. Miami: MedMaster IncHughes, D., Raghavan, A., Mordekar, S., Griffiths, P., & Connolly, D. (2010). Role of imaging in the diagnosis of acute bacterial meningitis and its complications. Postgraduate Medical Journal, 86(1018), 478-485. , P., Azad, R., Prasad, K., Jha, S., Pradham, S., & Gupta, R. (2004). Infectious meningitis: Prospective evaluation with magnetization transfer MRI. British Journal of Radiology, 77, 387-394. , J., & Wartofsky, L. (2012). Thyroid Emergencies. Medical Clinics of North America, 96, 385-403. , D. (2013). Cerebrospinal fluid (CSF) analysis- meningitis. GlobalRPh: The Clinician’s Ultimate Reference. Retrieved from , M., & Wilde, J. (2012). Viral meningitis: Which patients can be discharged from the emergency department?. The Journal of Emergency Medicine, 43(6), 1181-1187. , B., & Burman, K. (2006). Thyrotoxicosis and thyroid storm. Endocrinology and Metabolism Clinics of North America, 35, 663-686. Board of Nursing. (2013). The formulary developed by the committee on prescriptive governance. Ohio Board of Nursing, 1-36. Retrieved from nursing.Pietrobon, D., & Striessnig, J. (2003). Neurobiology of migraine. Nature Reviews: Neuroscience, 4, 386-399. , W. (2013). Aneurysmal subarachnoid hemorrhage. Nursing 2013, 42-51. Retrieved from Seehusen, D., Reeves, M., & Fomin, D. (2003). Cerebrospinal fluid analysis. American Family Physician, 68(6), 1103-1109. Retrieved from , S., & Dodick, D. (2013). Migraine genetics- A review Part I. Headache: The Journal of Head and Face Pain, 1-11. , A., Hartman, B., Kaplan, S., Kaufman, B., Roos, K., Scheld, M., & Whitley, R. (2004). Practicing guidelines for the management of bacterial meningitis. Clinical Infectious Diseases, 39, 1267-1284. Retrieved from 1Thyroid Storm Diagnostic CriteriaDiagnostic ParametersScoring PointsThermoregulatory DysfunctionTemperature99-99.95100-100.910101-101.915102-102.920103-103.925≥104.030Central Nervous System EffectsAbsent0Mild (Agitation)10Moderate (Delirium, Psychosis, Extreme Lethargy)20Severe (Seizures, Coma)30Gastrointestinal-Hepatic DysfunctionAbsent0Moderate (Diarrhea, Nausea, Vomiting, Abdominal Pain)10Severe (Unexplained Jaundice)20Cardiovascular DysfunctionTachycardia90-1095110-11910120-12915≥14025Congestive Heart FailureAbsent0Mild (Pedal Edema)5Moderate (Bibasilar Rales)10Severe (Pulmonary Edema)15Atrial FibrillationAbsent0Present10Atrial Fibrillation with Precipitating EventAbsent0Present10Table 1. Adapted from: (1) B. Nayak & K. Burman. (2006). Thyrotoxicosis and thyroid storm. Endocrinology and Metabolism Clinics of North America, 32, 663-686. ................
................

In order to avoid copyright disputes, this page is only a partial summary.

Google Online Preview   Download