case studies 3 and 4 - laura j. langenhop rn, bsn,...

Running head: langenhop_CASE STUDIES 3 AND 4 1

Case Studies 3 and 4

Laura Langenhop

Wright State University

langenhop_CASE STUDIES 3 AND 4 2

Case Studies 3 and 4

1.Which of the following processes can produce postoperative hypotension? Explain your

rationale. Bold the correct answer.

A. Hypovolemia secondary to blood loss

B. Sepsis

C. Adrenal insufficiency

D. Perioperative myocardial infarction

E. All of the above

Post-operative hypotension can occur through multiple channels. Hypovolemia, sepsis,

adrenal insufficiency, and perioperative myocardial infarction are processes that can produce

postoperative hypotension. Hypovolemia secondary to acute blood loss can produce post-

operative hypotension. An increase in blood loss causes the body to compensate with

tachycardia in order to maintain an adequate cardiac output (Laine, 2012). Tachycardia can only

persist for a certain amount of time before the body decompensates and hypotension occurs. A

decrease in hemoglobin and hematocrit may not decrease initially, but can occur over a period of

72 hours after the acute blood loss as extravascular volume travels into the vascular space (Laine,

2012). Hypovolemia is common following surgery when acute blood loss and extravascular

volume manifest (Laine, 2012). If left untreated, hypotension can occur.

Sepsis has been known to cause hypotension. Reasons are multifactorial. First,

myocardium dysfunction occurs in 40% of patients and can be systolic, diastolic, or biventricular

in nature (Ely & Goyette, 2005). Myocardium dysfunction occurs with the release of cytokines

and TNF-alpha mediators causing myocardial ischemia followed by reperfusion injury (Ely &

Goyette, 2005). Myocardial dilation, ventricular changes, and changes on a patient’s


electrocardiogram are suspected to be potential consequences of myocardial dysfunction with

subsequent hypotension (Ely & Goyette, 2005).

The common response from a person with hypotension is vasoconstriction of the

systemic vasculature. In sepsis, a patient is in a state of vasodilation. Blood vessels are unable

to properly respond to vasopressors and intravenous fluids causing hypotension (Ely & Goyette,

2005). Nitric oxide in the smooth muscle and endothelium are increased by cytokine activity,

causing increased vasodilation and decreasing systemic vascular resistance ultimately causing

continued hypotension (Ely & Goyette, 2005).

The adrenal gland is important to the hemodynamic stability of a patient. The adrenal

cortex releases mineralocorticoids and glucocorticoids in order for glucose to be more readily

available and for extracellular volume to be sustained (Marino, 2014). The adrenal medulla

releases catecholamines in order to stabilize circulation (Marino, 2014). Adrenal insufficiency

can be dormant until a physiologic stressor such as surgery or infection occurs. When patients

have adrenal insufficiency, they can become hemodynamically unstable with hypotension being

one of the signs (Marino, 2014). Adrenal insufficiency can be due to the inhibition of the

hypothalamic-pituitary level or inhibition of the adrenal gland. When adrenal insufficiency is

present, the patient experiences hypotension (Marino, 2014).

A perioperative myocardial infarction can occur without symptoms when a patient is

under anesthesia, while at the same time electrocardiogram and creatine-kinase levels have the

inability to be specific and sensitive in their testing because of the co-existence of muscular

injury from surgery (Landesberg, Beattie, Mosseri, Jaffe, & Alpert, 2009). A perioperative

myocardial infarction develops within two to three days of surgery and is detected between day

three and five following surgery (Landesberg et al., 2009). Tachycardia is the most common


cause of oxygen demand perioperatively. Following a surgical procedure, hypovolemia and

bleeding can cause hypotension due to increased myocardial demand. A myocardial infarction

increases the demand on the myocardium and decreases the supply of oxygen throughout the

body (Landesberg et al., 2009). Ischemia and hypervolemia leads to myocardial decompensation

subsequently producing hypotension (Landesberg et al., 2009).

2. Which of the following is the most appropriate method to diagnose BMAH? Explain

your answer.

A. Cortrosyn stimulation test

B. CT scan of adrenal glands

C. CT scan of adrenal glands and Cortrosyn stimulation test

D. Random plasma cortisol level

The first method in diagnosing bilateral massive adrenal hemorrhage is a computed

tomography (CT) scan of the adrenal glands. A CT scan of the adrenal glands is a quick and

reliable test for the diagnosis of BMAH (Green & Cohen, 2010). In the instance of BMAH, the

adrenal glands have an oval shape, are hyper-dense in structure, and appear to be between two to

five centimeters in diameter (Green & Cohen, 2010). The adrenal glands’ crura are thickened.

There is reduction in size and density over time. A CT scan of the adrenal glands will show

enlarged adrenal glands with high attenuation (Green & Cohen, 2010; Liew et al., 2012).

A Cortrosyn stimulation test is another reliable test in confirming the diagnosis of

BMAH. The hypothalamus produces a corticotrophin-releasing hormone that in turn causes that

anterior pituitary gland to release adrenocorticotrophic hormone (ACTH), producing activity of

the adrenal gland (Marino, 2014). Cortisol is therefore released from the adrenal cortex. Normal

production of cortisol is 15-25 mg/day in a normal non-stressed individual and up to 350 mg/day


for a patient under physiologic stress (Marino, 2014). In patients who remain hypotensive in

spite of fluid resuscitation and vasopressor initiation, the diagnosis of adrenal insufficiency

should be suspected (Marino, 2014).

An ACTH stimulation test is completed by first drawing the patient’s cortisol level at

baseline. A baseline cortisol level less that 10 mcg/dL is evident of adrenal insufficiency

(Marino, 2014). The patient is then given an intravenous synthetic ACTH dose. After an hour of

the ACTH administration, another cortisol level is drawn. If the cortisol level does not increase

more that 9 mcg/dL of the baseline cortisol level, suspicion of adrenal insufficiency should be

considered (Marino, 2014).

3. Which of the following can occur in patients with primary adrenal insufficiency?

Explain your answer.

A. Electrolyte abnormalities

B. Hypotension

C. Mental status change

D. Abdominal pain

E. All of the above

Electrolyte abnormalities, hypotension, mental status change, and abdominal all occur in

primary adrenal insufficiency. The first issue that can arise from adrenal insufficiency is

electrolyte abnormalities. The adrenal gland is divided into the outer cortex and the inner

medullary zone (Tucci & Sokari, 2014). The adrenal cortex is subdivided into the zona

fasiculata, zona reticularis, and zona glomerulosa (Tucci & Sokari, 2014). The zona fasiculata

and zona reticularis produce glucocorticoids and androgens. The zona glomerulosa produces


mineralcorticoids. The most important mineral-corticoid produced is aldosterone (Tucci &

Sokari, 2014).

In the presence of adrenal insufficiency aldosterone production is decreased. Inadequate

levels of aldosterone released from the adrenal gland cause hypovolemia, hyponatremia,

hyperkalemia, and hypotension (Lin & Denker, 2012). In patients with primary adrenal

insufficiency, 80% have hyponatremia and 40% have hyperkalemia (Arlt, 2012). The decrease

in aldosterone primarily causes hyponatremia. The inability to release anti-diuretic hormone

results in a mild form of Syndrome of Inappropriate Secretion of Anti-Diuretic Hormone

(SIADH) (Arlt, 2012). Hypercalcemia is also common in untreated adrenal insufficiency due to

the uptake of calcium in the renal tubule and gut (Arlt, 2012).

Hypotension also occurs in patients with adrenal insufficiency. Hypotension occurs as a

result of decreased myocardial contractility as well as a decreased response to catecholamines

(Liew, Sheehy, Wood, & Coursin, 2012). The glucocorticoids released by the adrenal gland

facilitate catecholamine release, such as norepinephrine and epinephrine, in order to maintain

blood pressure. Cardiovascular integrity also is a result of proper glucocorticoid release (Liew et

al., 2012). When an improper amount of glucocorticoids is released cardiovascular integrity is

compromised and ultimately hypotension occurs (Liew et al., 2012). Postural hypotension may

progress to hypovolemic shock in patients if left untreated (Arlt, 2012).

Adrenal insufficiency also mimics vague symptoms of acute abdominal pain, abdominal

tenderness, fever, nausea, and vomiting (Arlt, 2012). In some cases, patients present to the

emergency department with decreased levels of consciousness that can quickly worsen to a coma

(Arlt, 2012). Changes in mental status in patients with primary adrenal insufficiency are likely

related to abnormal electrolytes. Hyponatremia alone has been known to cause mental status


changes in individuals (Arlt, 2012). Surgery, illness, infection, or an increase in glucocorticoid

inactivation can cause an adrenal crisis (Alrt, 2012). Treatment of such a crisis requires volume

resuscitation, glucocorticoid initiation, and continuous hemodynamic monitoring (Arlt, 2012).

4. Which of the following is not a risk factor for developing BMAH? Explain your

rationale.

A. Postoperative state

B. Coagulopathy

C. Thromboembolic disease

D. Diabetes

E. Sepsis

There are often multifactorial reasons why a patient can experience bilateral massive

adrenal hemorrhage (BMAH). The adrenal gland receives blood flow from the phrenic artery,

adrenal artery, and the subcapsular plexus (Egan, Larkin, Ryan, & Waldron, 2009). Adrenal

hemorrhage can occur from hypotension, vascular engorgement, and vascular stasis (Egan et al.,

2009). Diabetes is not a risk factor for developing bilateral massive adrenal hemorrhage.

Postoperative state, coagulopathy, thromboembolic diseases are risk factors for BMAH. Like

sepsis, following surgery there is an inflammatory response that occurs within the body. Adrenal

insufficiency in a postoperative patient occurs when the body is unable to produce adequate

amounts of cortisol in the face of acute stress (Marik & Zaloga, 2005).

In a patient with heparin-induced thrombocytopenia (HIT), coagulopathy is a risk factor

for BMAH. Patients with HIT experience a decrease in platelet levels following administration

of heparin or low-molecular weight heparin following surgery or for deep vein thrombosis

prophylaxis (Rosenberger et al., 2011). HIT is mediated by an antibody effect. The patient may


experience a 50% drop in platelets as well as a formation of a new thrombus within 14 days of

the heparin administration (Rosenberger et al., 2011). The patient becomes prone to a

hypercoaguable state. Risk for hemorrhage as well as bleeding is increased. The adrenal gland

promotes an atmosphere of venous and arterial thrombosis leading to a high risk of BMAH

(Rosenberger et al., 2011).

Thromboembolic disease, as with Antiphospholipid Syndrome (APS), is another risk

factor for adrenal hemorrhage (Silverio, Caetano, Gomes, & Sequeira, 2012). Two mechanisms

have been proposed as the rationale behind adrenal hemorrhage in the presence of

thromboembolic diseases. The first is that the adrenal gland is rich in arterial supply and lacks in

venous drainage. Because of the physiology of adrenal gland, there is risk for pockets of

turbulence and local stasis of blood (Silverio et al., 2012). In the event of thrombosis, arterial

blood pressure in the affected area increases, followed by hemorrhaging.

The second mechanism is that the adrenal gland cells are rich in cholesterol (Silverio et

al., 2012). In patients with APS, production of antibodies that attack lysobiphosatidic acid in the

adrenal cortex causes an increase in cholesterol, the release of lysosomal proteinases, endothelial

dysfunction and the production of small thrombi (Silverio et al., 2012). The thrombi travel, like

in the first mechanism, leading to increased arterial pressure in the adrenal arteries resulting in

hemorrhage (Silverio et al., 2012).

Sepsis is also a risk for adrenal insufficiency. It has been reported that up to 60% of

patients with severe sepsis and septic shock develop adrenal insufficiency (Marino, 2014).

Patients with sepsis suffer from critical illness-related corticosteroid insufficiency. During

sepsis, an inflammatory response occurs throughout the whole body. There is suppression of the


hypothalamus and pituitary gland causing adrenal insufficiency (Marino, 2014). Therefore, a

patient with sepsis is at a higher risk of developing adrenal insufficiency (Marino, 2014).

5. Which of the following statements regarding the long-term management of patients with

BMAH is correct? Explain your answer.

A. Glucocorticoid therapy is needed only during acute illness

B. Patients should be discharged on maintenance doses of oral glucocorticoids and

mineralocorticoids.

C. Patients do not need mineralocorticoid therapy.

D. Adrenal function is likely to recover over 4 to 6 months with no further need for

glucocorticoids.

Patients with bilateral massive adrenal hemorrhage should be discharged on both

maintenance doses of oral glucocorticoids and mineral-corticoids. Initially, if adrenal crisis is

suspected, a bolus dose of hydrocortisone should be administered. Hydrocortisone is then

prescribed every six hours for a total dose of 300 mg/day (Rosenberger et al., 2011). Once

symptoms and hemodynamics stabilize, the patient may begin taking an oral regimen.

Glucocorticoids are prescribed at morning and at nighttime to mimic cortisol secretion.

Hydrocortisone is typically prescribed between 15-25 mg in order to resemble the daily cortisol

production (Liew et al., 2012). Prednisolone and Dexamethasone may be ordered in place of

hydrocortisone for patients who are non-compliant or who experience afternoon fatigue. In the

state of Ohio, the advanced practice registered nurse (APRN) can prescribe glucocorticoids (The

Ohio Board of Nursing, 2014).

Mineralcorticoids, such as Fludrocortisone (Florinef), are initiated and maintained at a

dose of 0.1mg/day (Liew et al., 2012). Mineralcorticoids promote reabsorption of sodium and


loss of potassium in the renal distal tubules (Rosenberger et al., 2011). Side effects of this

medication are hypertension, edema, and hypokalemia. It is important to monitor electrolytes,

plasma renin, and blood pressure when prescribing these medications (Liew et al., 2012). In the

state of Ohio, the advanced practice registered nurse (APRN) can prescribe glucocorticoids (The

Ohio Board of Nursing, 2014).

Case Study 4

A 46 year-old male comes into the emergency department complaining of nausea and

vomiting he has experienced over the past month. The patient states in the past 24 hours he has

started to vomit a small amount of bright red blood. The patient states the nausea and vomiting

persist throughout the day with no consistency in their presence. The patient’s nausea subsides

following consumption of a small amount of food. The patient denies being awakened during

the night with nausea. The patient does state he has abdominal pain described as “achy” and

“gnawing” in the epigastric area. The patient does admit to feeling fatigued. The patient has

taken over the counter ibuprofen 400 mg for the pain every six hours for the past couple of

weeks with minimal relief. The patient states his stool has not changed in consistency or color

over the past month. The patient denies taking any prescribed medications currently. The

patient admits to drinking between two to three glasses of coffee a day. The patient is a

vegetarian and states he eats healthy. There has been no unplanned weight loss or weight gain

within the last month. The patient is a social drinker, drinking two glasses of wine a week. The

patient states he recently changed jobs. The patient traveled to the Caribbean on a cruise where

he visited three different islands one month prior to admission. The patient denies being sexually

active. Physical examination reveals active bowel sounds. There is no pain on light, moderate

and deep palpation. There is negative murphy and McBurney’s signs. The patient’s last bowel


movement was this morning. Test results as are follows: WBC 8.5, RBC 4.69, H/H 8.2/26,

Platelets 226, Na 139, K 4.1, Cl 105, CO2 26, BUN 16, Cr. 1.38, Ca 9.4, INR 1.0. Urinalysis

was negative. Abdominal ultrasound was negative for acute bleed of cholelithiasis. Vital signs

are as follows: 97.9 Fahrenheit, HR 110 normal sinus rhythm, BP 98/60, RR 16, SpO2 96% on

RA.

1. What are the differential diagnoses for this patient?

The differential diagnoses for this patient are peptic ulcer disease (PUD),

gastroesophogeal reflux disease (GERD), acute gastritis, gastric ulcer, esophagitis, and acute

gastrointestinal bleed. Peptic ulcer disease is the first differential diagnosis for this patient. A

peptic ulcer is a tear in the gastric or the duodenal mucosa. The tear occurs due to an increased

amount of acid and pepsin (Valle, 2012). Men between the ages of 30 and 55 years of age and

patients taking non-steroidal anti-inflammatory drugs (NSAIDS) are at an increase risk of

developing peptic ulcer disease (Valle, 2012).

Peptic ulcer disease (PUD) originates from an imbalance of the protective and aggressive

factors of the gastrointestinal tract (Lew, 2012). In the presence of gastrin and pepsin, the

patient’s defense mechanisms are impaired. Ulcers form causing discomfort in the epigastric

area. In patients with peptic ulcer disease, complaints of burning, dull, and gnawing pain are

present (Lew, 2012). Burning subsides by consuming food. In this specific case study, the

symptoms of burning pain and nausea subside with food consumption. The patient also has a

long-standing history of taking NSAIDs for headache with increased consumption for his

abdominal pain. The last possible issue the patient may be dealing with is Helicobacter Pylori

(H. Pylori) causing the patient’s peptic ulcer disease. The patient recently went on a cruise and

explored different countries, consuming meals in various places. H. Pylori can develop through


an oral to oral or fecal to oral route (Ferri, 2015). One must consider the possibility of the

patient developing H. Pylori based on his recent travels. The patient’s most likely diagnosis is

peptic ulcer disease (Lew, 2012).

There are 400,000 Americans that are admitted each year to the hospital with upper

gastrointestinal bleeding related to PUD (Tintanalli et al., 2011). Isotonic saline, packed red

blood cells, and a proton pump inhibitor infusion are warranted at times when hemodynamic

instability is seen. It is at times hard to differentiate between peptic ulcer disease and acute

gastritis. The major difference in these two states is that gastritis often comes with a massive

upper gastrointestinal bleed, whereas PUD does not. PUD also is almost always described as a

burning pain in the epigastric area (Tintanalli et al., 2011). The patient’s symptoms in this case

study are more consistent with peptic ulcer disease.

Infection is the most common cause of acute gastritis (Valle, 2012). Unlike the patient in

this case study, acute gastritis is associated with a sudden onset of epigastric pain, nausea, and

vomiting (Valle, 2012). Neutrophils, hyperemia, and edema are noted on the histology report of

these patients. Elderly individuals, alcoholics, and immunocompromised patients may be

affected by gastritis. Other causes of acute gastritis are polypectomy and mucosal injection with

India ink (Valle, 2012). Streptococci, staphylococci, escherichia coli, proteus, and haemophilus

species are all common pathogens for acute gastritis. Though acute gastritis is a possible

diagnosis in this case study, given the time frame and onset of symptoms, there is most likely

another cause of this patient’s dyspepsia (Valle, 2012).

Esophagitis is considered to be inflammation of the esophagus proceeded either by

GERD or infiltrates from the mucosa caused by a food allergy (Bennett, Dolin, & Blaser, 2015).

Patients who are immunocompromised are predominantly those who are affected by esophagitis.


Rarely will a patient who is otherwise healthy get esophagitis. Typical pathogens include

candidiasis, cytomegalovirus, herpes simplex virus, and human immunodeficiency virus

(Bennett, Dolin, & Blaser, 2015). Non-infectious forms of esophagitis are caused by GERD,

ingestion of corrosives, long-standing use of NSAIDS, and mucositis from medications such as

antibiotics that come in capsule form (Bennett, Dolin, & Blaser, 2015). Patients will present to

the emergency department or primary care offices with complaints of pain with swallowing.

Patients can experience worsened pain by eating foods that are high in acid. Weight loss,

nausea, and vomiting are other common presented signs and symptoms. In this specific case, the

patient does not have pain on swallowing or difficulty swallowing. The patient does however

have a history of taking NSAIDS as well as nausea and vomiting, so the diagnosis cannot be

ruled out without imaging. The patient is also not immunocompromised and does not have a

history of GERD making this diagnosis rare (Bennett, Dolin, & Blaser, 2015).

Acute gastrointestinal bleed is the last differential diagnosis. The patient in this case

developed hematemesis following a month of nausea and vomiting. Upper gastrointestinal

bleeding occurs from many different disease states. Peptic ulcer disease, portal hypertension,

vascular anomalies, Mallory Weiss tears, gastritis, and esophagitis are a few common causes of

acute gastrointestinal bleeding (McQuaid, 2014). Patients can present with tachycardia and

hypotension, revealing to the provider severe acute blood loss. Resuscitation efforts with

isotonic saline and packed red blood cells should be administered in order to prevent further

compromise of the patient’s hemodynamic instability. The patient in this case has a lower

hemoglobin and hematocrit with tachycardia reflective of a more severe acute GI bleed

(McQuaid, 2014). Proper fluid resuscitation should be performed to stabilize the patient. Once

the patient is stable, the focus can be on the causes of the bleeding.


2. What are the two major causes of peptic ulcer disease?

The two major causes of peptic ulcer disease are long-term use of non-steroidal anti-

inflammatory medications and H. Pylori (McQuaid, 2014). Within a year there is a two to five

percent likelihood of a duodenal ulcer originating from long-term NSAID use causing serious

complications (Ferri, 2015). Patients who are at risk for serious complications are patients taking

NSAIDs in combination with aspirin, anticoagulants, or corticosteroids (Valle, 2012). NSAIDs

inhibit prostaglandins by reversing the inhibition of COX-1 and COX-2 enzymes. Aspirin also

causes inhibition of COX-1 and COX-2 enzymes as well as platelet aggregation. The issue with

COX-1 enzymes is they cause a cytoprotection to the mucosal lined layer of the stomach and

duodenum. As the enzymes that protect the layer are inhibited, the risk for ulcer is increased

(Laine, 2012). The use of aspirin alone doubles the risk of developing bleeding in a patient with

peptic ulcer disease.

H. Pylori increases the risk of peptic ulcer disease by three times when the patient is

taking NSAIDs or aspirin (Ferri, 2015). The etiology of H. Pylori is unknown, but most believe

it originates from oral to oral or fecal to oral route. Food contamination is also a possibility. H.

Pylori invades the mucosal layer of the duodenum and gastric area causing vulnerability to acid

peptic damage (Ferri, 2015). It is important to detect signs and symptoms of H. Pylori early as

well as obtain a proper history and physical in order to prevent malignancies from arising (Ferri,

2015).

3. What imaging/testing should be ordered for this patient?

The gold standard for the diagnosis of peptic ulcer disease is an esophagoduodenoscopy

(EGD). The sensitivity and specificity are greater than 95% for visualization of an ulcer, and

endoscopy allows the viewing of other potential abnormalities and allows biopsy of appropriate


lesions (Laine, 2012). Also, an EGD is more sensitive and specific than barium studies of the

upper gastrointestinal system (McQuaid, 2014). During an EGD, the physician is looking for

sources of bleeding, malignancy ulcers, and esophagitis (McQuaid, 2014).

The patient in this case study will have an EGD completed because of the acute GI bleed.

The patient also had recent travel outside of the country placing him at risk for ingesting

contaminated food. With a possible diagnosis of H. Pylori, the gastroenterologist will order

histology, rapid urease testing, culture and polymerase testing. In a patient that does not have an

active GI bleed and shows no evidence of bleeding, an EGD may not be recommended (Chey &

Wong, 2007). In this case, the nurse practitioner will order antibody testing, urea breath tests,

and fecal antigen tests. The antibody testing is widely used and has a good negative predictive

value (Chey & Wong, 2007). Urea breath tests have a great positive and negative predictive

value regardless of H. Pylori prevalence, however reimbursement for this testing and availability

are not consistent (Chey & Wong, 2007). Fecal antigen testing also tests active H. Pylori

infection with good negative and positive predictive value (Chey & Wong, 2007). Fecal antigen

testing is also convenient for follow-up appointments (Atherton & Blaser, 2012).

The urea breath test is an accurate way of identifying H. Pylori if the patient has not been

prescribed a PPI within the last two weeks prior to the EGD. A urea breath test is inexpensive

and does not require an EGD (Atherton & Blaser, 2012). Histology with biopsies should be

taken in a patient who has been taking a PPI. A urea breath test does not need to be performed on

the individual since the test results will be skewed (Chey & Wong, 2007). The sensitivity of the

urea breath test can decreased by 25% if a patient has been taking a PPI, bismuth, and antibiotics

(Chey & Wong, 2007). Culturing during an EGD results in highly specific testing, but is not as

sensitive as the rapid urea breath tests and histology (Chey & Wong, 2007). Finally, a


polymerase chain reaction (PCR) can also be completed with high specificity for H. Pylori. A

PCR has been shown to detect up to 20% on H. Pylori cases from gastric biopsies (Chey &

Wong, 2007).

In the event that the patient has symptoms of bowel perforation, penetration, or

obstruction from peptic ulcer disease, a computed tomography (CT) scan should be obtained

(Laine, 2012). The specificity of a CT scan to rule-out bowel obstruction, penetration, or

perforation is 95% with a sensitivity of 64% (Zissin, Osadchy, & Gayer, 2009). Though not a

first choice in testing peptic ulcer disease, a CT scan can be done to rule out complications of

surrounding organs (Laine, 2009; Zissin, Osadchy, & Gayer, 2009).

4. What are the treatment options for this patient?

Stabilization of this patient is the first step in treatment. In a patient with active bleeding,

two 18-gauge large bore intravenous catheters should be inserted for proper resuscitation with

isotonic saline and packed red blood cells. In a patient with a coagulopathy, reversal of certain

clotting factors may be warranted. A proton pump inhibitor infusion is typically started in order

to aid in the suppression of gastric or duodenal ulcers that have formed (Ferri, 2015). As stated

above, an EGD should be completed within 24 hours of hospital admission in order to diagnose

the peptic ulcer as well as to biopsy if necessary (Chey & Wong, 2007). Once a patient is

diagnosed with peptic ulcer disease associated with NSAID use, the next step is to stop

medications that are causing the ulcer (Chey & Wong, 2007). NSAIDs should be stopped. This

patient takes in a moderate amount of coffee a day and a moderate amount of alcohol a week.

Education on the benefits of reducing caffeine and alcohol intake can lead to decreased acid

production and symptoms (McQuaid, 2014).


In patients with a diagnosis of peptic ulcer disease, with no sign of H. Pylori, a proton

pump inhibitor (PPI) is the recommended drug of choice in treating these patients (McQuaid,

2014). Proton pump inhibitors bind to the acid-secreting enzymes and cause malfunction and

inactivation. After four weeks of treatment with a PPI, 90% of duondenal ulcers have been

shown to effectively heal whereas 90% of gastric ulcers have been shown to heal after eight

weeks (McQuaid, 2014). The other treatment choice for PUD is an H2-receptor antagonist.

Unfortunately, H2-receptor antagonists are not the drug class of choice in treating peptic ulcer

disease. Proton pump inhibitors suppress 90% of acid secretion in a one day, whereas H2-

receptor antagonists only suppress 65% (McQuaid, 2014). Therefore it is recommended to

prescribe a proton pump inhibitor for four weeks in a patient with peptic ulcer disease. If given

PPIs for longer than recommended treatment, the advanced practice registered nurse should be

aware of the effects on the patient. Long-term use can cause a decreased Vitamin B12, iron, and

calcium absorption and place patients at risk for clostridium difficile (McQuaid, 2014; Chey &

Wong, 2007). In the state of Ohio, the advanced practice registered nurse can prescribe proton

pump inhibitors and H2-receptor antagonists (The Ohio Board of Nursing, 2014).

The first line combination of medications to administer to this patient is a PPI twice daily,

500 mg of Clarithromycin twice daily, and one gram of amoxicillin twice daily for 10 to 14 days

(Chey & Wong, 2007). Metronidazole can be substituted for amoxicillin in patients with

penicillin allergy. Another alternative treatment is 525 mg of bismuth subsalicylate four times a

day, metronidazole 250 mg four times a day, tetracycline 500 mg four times a day, ranitidine 150

mg twice daily, and a PPI twice daily prescribed orally and for 10-14 days. The triple therapy

combination has been shown to eradicate the disease by 75-90% (Chey & Wong, 2007). In the


state of Ohio, the advanced practice registered nurse can prescribe the triple and quadruple

therapy for patients with H. Pylori (The Ohio Board of Nursing, 2014).


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