Download In-Class/Online Case Study Brief Patient History: Mr. C is a 38

IN-CLASS/ONLINE CASE STUDY
Brief Patient History:
Mr. C is a 38-year-old Hispanic male admitted to the intensive care unit from the emergency department
(ED) in hypovolemic shock. Mr. C was initially diaphoretic, unresponsive, and pale with a blood pressure
of 70 systolic. After fluid resuscitation in the ED, his blood pressure increased to 90 systolic and
responsiveness was restored. Mr. C is a migrant worker from Mexico who speaks limited English and is
married with four children. All family members live in Mexico, except his uncle. Mr. C’s uncle verbalizes
that his nephew has been complaining of severe abdominal pain for the past few days, with frequent
episodes of nausea and vomiting.
Clinical Assessment:
Mr. C is in a fetal position, complaining of nausea and intolerable knifelike abdominal pain, radiating to his
back. A physical examination reveals that Mr. C is restless, obeys commands, and moves all extremities.
Bilateral breath sounds are diminished with bibasilar crackles, S1 S2 without murmur, and capillary refill
greater than 3 seconds, and peripheral pulses are 1+. Abdomen is distended and tenderness and
guarding, hypoactive bowel sounds, and tympany are noted. Trousseau’s sign (carpopedal spasm with
inflation of blood pressure cuff) and Chvostek’s sign (muscle spasm of the face with tap on facial nerve)
are present. Skin is cool, pale, and dry. IV fluids are Ringer solution at 200 mL/hr and Foley catheter
draining amber urine at 20 mL/hr.
Diagnostic Procedures:
Mr. C’s vital signs include blood pressure of 92/68 mm Hg, pulse of 122 beats/min that is thready and
weak, respiratory rate of 26 breaths/min, temperature of 100.8° F, and SpO2 of 92% on O2 at 4 L per
nasal cannula. His arterial blood gasses are: pH of 7.48, PaO 2 of 80 mm Hg, PaCO2 of 48 mm Hg, HCO3
level of 38 mEq/L. He has an O2 saturation of 95% on an FIO2 of 36%.
Diagnostic values for Mr. C are as follows:
WBC, 19,600 units/L; hematocrit (Hct), 48.3%; hemoglobin (Hgb), 11.6 g/dL;
blood urea nitrogen (BUN), 18 mg/dL; serum creatinine, 1.2 mg/dL; serum glucose, 220 mg/dL; serum
amylase, 280 Somogyi units/mL; serum lipase, 13.5 Somogyi units/mL; serum sodium, 140 mEq/L; serum
potassium, 2.9 mEq/L; serum calcium, 5.8 mg/dL; serum albumin, 2.8 mg/dL; serum magnesium, 0.9
mg/dL; serum C-reactive protein, 140 mg/dL; and serum lactate, 3 mmol/L.
Medical Diagnosis
Acute Pancreatitis/Ranson criteria of 4
1. What major outcomes do you expect to achieve for this patient?
Answer: Major outcomes for Mr. C include: (1) adequate fluid balance and tissue perfusion; (2)
relief of pain; (3) optimal nutrition; (4) electrolytes and glucose values are within normal; (5)
optimal communication; (6) reduction of anxiety and fear; and (7) free of local and systemic
complications associated with pancreatitis.
2. What problems or risks must be managed to achieve these outcomes?
Answer:
a. Fluid volume deficit and impaired tissue perfusion are seen in the patient with pancreatitis due to
massive fluid loss up to 6 to 8 L into the peritoneal region, and hypovolemia that occurs with nausea
and vomiting. Mr. C’s blood pressure of 92/68 mm Hg, pulse of 122 beats/min that is thready and
weak, respiratory rate of 26 breaths/min, and urine output of 20 mL/hr reflect hypovolemic shock and
impaired tissue perfusion.
b. Pain control: Pain associated with pancreatitis is related to the edema, impaired perfusion, and
distention of the pancreas, and peritoneal distention and inflammation. Mr. C is in a fetal position,
complaining of intolerable knifelike abdominal pain that is radiating to his back. Pain management is a
priority for him.
c. Nutritional support: Nausea, vomiting, and increased metabolic demands place Mr. C at risk for
nutritional deficit.
d. Electrolytes and glucose imbalances: Hypocalcemia, hypomagnesium, hypokalemia, and
hyperglycemia are common imbalances for the patient with acute pancreatitis. Mr. C has all of these
imbalances as reflected in his diagnostic values, and his ABG reflects partial-compensated metabolic
alkalosis (pH of 7.48, PaCO2 of 48 mm Hg, HCO3 level of 38 mEq/L), reflective of upper
gastrointestinal fluid loss, and hypokalemia.
e. Communication/anxiety and fear: Mr. C’s limited English can be a major communication barrier,
which can lead to increased anxiety, fear, and isolation. A priority in nursing care is communication,
which is the foundation for all that nurses do. Communication barriers and communication problems
have been identified as the root cause of many “sentinel events,” medical errors, unnecessary costs,
and inadequate treatments; therefore, communication is critical in caring for all patients, especially
non-English-speaking and/or limited-English-speaking patients like Mr. C. Critical illness is a stressproducing event that leads to anxiety and fears in all patients and their families, and communication
barriers can exacerbate these anxieties and fears.
f. Local/systemic complications and multiple organ dysfunction syndrome (MODS):
Acute pancreatitis can affect every organ system, and therefore recognition and treatment of systemic
complications are crucial to management of the patient with pancreatitis and prevention of MODS.
Cellular destruction in pancreatic injury results in the release of toxic enzymes and inflammatory
mediators into the systemic circulation and causes injury to vessels and other organs distant from the
pancreas; this may result in systemic inflammatory response syndrome (SIRS), multiorgan failure, and
death. Local complications associated with pancreatitis involve widespread infection and inflammation
of the pancreas, which can lead to pancreatic necrosis and pancreatic pseudocyst. The necrotic
region of the pancreas and pancreatic pseudocyst may cause peritonitis (if rupture occurs) and/or
hemorrhage (if a major blood vessel erodes).
3. What interventions must be initiated to monitor, prevent, manage, or eliminate the problems
and risks identified?
Answer: Initial management of the patient with severe acute pancreatitis includes ensuring adequate
fluid and electrolyte replacement, providing nutritional support, and correcting metabolic alterations.
Careful monitoring for systemic and local complications is critical. Mr. C’s vital signs, cardiac rhythm,
and pulmonary status should be monitored and treated accordingly. Several prognostic scoring
systems have been developed to predict the severity of acute pancreatitis, so appropriate
management can be implemented. One of the most commonly used predictive tools of severity is the
Ranson criteria. If the patient has 0 to 2 factors present, the predicted mortality rate is 2%; with 3 to 4
factors, the predicted mortality rate is 15%; with 5 to 6 factors, the predicted mortality rate is 40%; and
with 7 to 8 factors, the predicted mortality rate is 100%. Mr. C has a Ranson criterion of 4 and thus a
predicted mortality of 15%. Critical monitoring and management of the following problems for Mr. C is
essential.
a. Fluid volume deficit and impaired tissue perfusion: Restoring fluid balance with 5 to 10 L of
intravenous crystalloids and colloids may be needed daily in the first few days to prevent hypovolemic
shock and maintain hemodynamic stability. Adequate tissue perfusion is evident by alert mental
status, lactate levels within normal limits, and urinary output of 0.5 mL/kg/hr or 30 mL/hr. Successful
fluid replacement is evaluated by hourly intake and output, daily weights, and stable heart rate, blood
pressure, and hemodynamic readings. Central venous pressures (CVP) of 8 to 12 mm Hg should be
attained. Low dose dopamine may be needed to maintain renal perfusion and support blood pressure.
Mr. C’s serum lactate of 3 should be monitored closely to assess for shock state and decrease in
perfusion. Lactate levels greater than 4 are indicative of an increased incidence of: (1) SIRS, (2)
MODS, and (3) mortality. Serum lactate is a good marker of severity of shock insult, and in predicting
survival.
b. Pain control: Pain management is a major priority in acute pancreatitis, not only due to the extreme
discomfort for Mr. C, but pain may increase pancreatic enzyme secretion and metabolic demand.
Essential to the plan of care for Mr. C are round-the-clock analgesics to achieve pain relief. Morphine,
fentanyl, and hydromorphone (dilaudid) are commonly used opiates administered IV for pain control.
Relaxation techniques, semi-Fowler position, and the knee-chest position can also assist Mr. C with
pain control.
c. Nutritional support: Over the past 3 decades, nutritional support has shifted. Previously,
conventional nutritional management was to place the patient on a nothing-by-mouth (NPO) regimen
and institute intravenous hydration. The rationale was to rest the inflamed pancreas and prevent
enzyme release. Enteral or parenteral support should be initiated if oral intake is withheld more than 5
to 7 days. Clinical trials have demonstrated that enteral feeding (gastric or jejunal) is safe, costeffective, and associated with fewer septic and metabolic complications than other methods. Enteral
feeding enhances immune modulation and maintenance of the intestinal barrier, and avoids
complications associated with parenteral nutrition. Early initiation of enteral feeding is preferred over
total parenteral nutrition (TPN); however, TPN still has a role for the critically ill patient with acute
pancreatitis who does not tolerate enteral feeding or when nutritional goals are not reached within 2
days. In the past, nasogastric suction was also recommended, but this intervention has not been
shown to be beneficial and should be instituted only if the patient has persistent vomiting, obstruction,
or gastric distention. Evidence-based practice recommends early enteral nutritional support for the
patient like Mr. C, with acute pancreatitis, to decrease complications and length of hospital stay.
Nutritional status is assessed by monitoring albumin, prealbumin, transferrin, glucose, cholesterol, and
triglyceride levels.
d. Electrolytes and glucose imbalances: Mr. C has hypocalcemia, hypomagnesium, and hypokalemia,
which will require replacement infusions of these electrolytes. The nurse must remember to follow
established protocols when administering infusions of calcium, potassium, and magnesium because of
the potential for cardiac dysrhythmias and venous irritation; therefore continuous cardiac monitoring of
the ECG is needed. Mr. C’s metabolic alkalosis (partial-compensation) should improve with potassium
and calcium replacement.
Serum calcium levels less than 8.5 mg/dL and hyperglycemia greater than200 mg/dL, with no diabetes
mellitus in the history, as seen in Mr. C’s diagnostic laboratory results, are associated with poor
outcome and higher mortality. Mr. C’s positive Chvostek and Trousseau signs reflect severe
hypocalcemia. Calcium levels less than 6 may lead to seizures and respiratory distress, requiring
seizure precaution and respiratory support equipment at bedside for Mr. C. Calcium replacement is a
priority, and monitoring Mr. C’s response to calcium replacement is necessary because of potential for
cardiac toxicity. The nurse must understand that calcium binds to serum albumin; therefore if the
albumin level is low, serum calcium values will be abnormally low and not reflective of true calcium
levels. A formula used in computing true calcium levels is the following:
• Total Ca (mg/dL) + 0.8 (4.0 − serum albumin [g/dL]) = true calcium level
(where 4.0 represents the average albumin level in g/dL)
• Mr. C’s calcium = 5.8 mg/dL + 0.96 = 6.76 mg/dL, Mr. C’s true calcium level
Hypocalcemia is also difficult to correct without first normalizing the serum magnesium concentration
and correcting the alkalosis. Mr. C’s hyperglycemia of 220 mg/dL also requires the administration of
exogenous insulin.
e. Communication/anxiety and fear: Health care providers from various disciplines and other staff who
interact directly with non-English-speaking and/or limited-English-speaking patients need to be trained
on how to communicate effectively. The health care provider should use interpreter and
communication boards to facilitate commonly used messages with these vulnerable patient
populations.
f. Systemic complications and multiple organ dysfunction syndrome (MODS): Acute pancreatitis as
stated can affect every organ system, and lead to MODS. The most serious complications are
hypovolemic shock, acute respiratory distress syndrome (ARDS), acute kidney injury (AKI), and
gastrointestinal hemorrhage. Hypovolemic shock is the result of relative hypovolemia resulting from
third spacing of intravascular volume and vasodilation caused by the release of inflammatory immune
mediators. These mediators also contribute to the development of ARDS and AKI. Other possible
pulmonary complications include pleural effusions, atelectasis, and pneumonia. Intensive monitoring
of each of the organ systems, per diagnostic studies, vital signs, hemodynamics, and ABGs, is
imperative because organ failure is a major indicator of the severity of the disease. Ms. C’s PaO 2 and
SaO2 should be monitored closely for early signs of ARDS, such as refractory hypoxemia in response
to oxygen administration. Each system must be supported early to prevent MODS. Mr. C should also
be closely monitored for signs and symptoms of pancreatic infection, which include increased
abdominal pain and tenderness, fever, and increased white blood cell count. Cullen sign (ecchymotic
discoloration of the umbilical region) and Grey Turner sign (ecchymosis of the flank region) may signal
severe hemorrhagic pancreatitis, with mortality estimated at 37%. Immediate intervention is needed
when these signs are assessed, which usually includes multiple blood transfusion, fresh-frozen
plasma, and/or surgical intervention to control the bleeding. The time to the appearance of the Cullen
or the Grey Turner sign is thought to be at least 24 hours after the onset of retroperitoneal bleeding
and averages about 3 days after the onset of pancreatitis. The appearance of ecchymoses in the
periumbilical area or flank had been taught as a hallmark of acute pancreatitis; however, these signs
are indicative of retroperitoneal bleed in many other conditions, including ruptured aortic aneurysm,
splenic rupture, complication of anticoagulation, and perforated duodenal ulcer, and as a manifestation
of liver disease.
4. What interventions should be initiated to promote optimal functioning, safety, and well-being
of the patient?
Answer: The goal of treatment is to relieve pain and minimize complications. Currently, no
medications are used to treat acute pancreatitis specifically. Therapy is primarily supportive and
involves intravenous (IV) fluid hydration, analgesics, antibiotics (in severe pancreatitis), and treatment
of metabolic complications (e.g., hyperglycemia and hypocalcemia).
The two most common causes of acute pancreatitis are gallstone migration and alcoholism. Together,
they account for approximately 80% of cases. Less common causes are quite diverse and include
surgical trauma, hypercalcemia, various toxins, ischemia, idiopathic infections, and the use of certain
medications. An abdominal ultrasound scan should be obtained as part of the diagnostic evaluation to
determine the presence of biliary stones. A contrast-enhanced computed tomography (CT) is
considered the gold standard for diagnosing pancreatitis and for ascertaining the overall degree of
pancreatic inflammation and necrosis.
Social and spiritual support is needed to help Mr. C cope with the effects of acute pancreatitis and
admission to a critical care unit. Since Mr. C’s wife and children are in Mexico, the nurse will need to
collaborate with patient care representatives, migrant leaders, and spiritual leaders to provide needed
support for Mr. C. Community resources need to be explored to see how Mr. C and his family can be
assisted. Optimal recovery will be impacted by needed social support from his family and home health
agencies.
5. What possible learning needs would you anticipate for this patient?
Answer: Early in Mr. C’s hospital stay, the patient and family members should be taught about acute
pancreatitis and its causes and treatment. As the patient moves toward discharge, teaching should
focus on the interventions necessary for preventing the recurrence of the precipitating disorder. If
sustained, permanent damage to the pancreas has occurred, Mr. C will require teaching specific to
diet modification and supplemental pancreatic enzymes. A low-fat diet is recommended to minimize
worsening or aggravating pancreatitis and to minimize fatty or oily stools, as the pancreas is the major
organ responsible for digestion of fat. Mr. C should also limit intake of fried foods, nuts, seeds, oils,
high-fat snacks, and desserts. A pancreatitis diet should include 6 to 8 small frequent meals/snacks,
rather than three full meals, to avoid overexerting the pancreas with a large amount of food at one
time. Pancreatic enzymes may be needed for chronic pancreatitis and malabsorption. Pancreatic
enzymes are taken with meals to enhance digestion and prevent malabsorption. It is also important to
ensure that Mr. C’s diet provides enough fluid to stay well hydrated, if malabsorption problems
develop. Diabetes education may also be necessary. Finally and very important, if Mr. C is an alcohol
abuser, he should be encouraged to stop to prevent further damage to his pancreas.
6. What cultural and age-related factors may have a bearing on the patient’s plan of care?
Answer: Migrant farmworkers represent one of the most marginalized and underserved populations in
the United States. The overriding dialogue surrounding immigration policy addresses the strain
immigrants put on all social systems, including health care. However, migrant farmworkers who
contribute to the agricultural system that feeds Americans deserve assistance in pursuit of health care.
Migrant farmworkers and families are separated from the greater community by social, cultural, and
language barriers, as well as by geographic location. Most migrant farmworkers live in inadequate
housing that is out of the sight of most community members. Lack of transportation and little free time
also isolates the population. As a group, migrant and seasonal farmworkers face significant language
barriers—about 9 in 10 say they read and speak little or no English. They are predominantly male
(88%), over half are married (52%), and over 4 in 10 have children (44%). Anxiety and depression
among migrant farmworkers are linked to family dysfunction, ineffective social support, hopelessness,
and high acculturative stress. Primary socialization can revolve around alcohol once the workday is
over. Alcoholism is a part of daily life for farmworkers, and alcohol is available even when food is not
readily available, because alcohol vendors come around the barracks in trucks. Isolation from family
and friends results in feelings of anguish, as may be the case in Mr. C’s situation. Programs and
policies are necessary to support migratory families such as Mr. C’s and offset social isolation as a
means to address the problem drinking and/or alcoholism that may be the precipitating cause of Mr.
C’s pancreatitis. Most migrant works are not even aware of services that may be available. Overall,
Hispanics are less likely to drink than are non-Hispanic whites. In fact, Hispanics have high rates of
abstinence from alcohol. But Hispanics who choose to drink are more likely to consume higher
volumes of alcohol than non-Hispanic whites and have a greater percent of complications associated
with alcohol (cirrhosis, pancreatitis, accidents, and violence). Mexican Americans/Hispanics exhibit
strong family ties. They love and take care of their family and love to socialize among their vast
extended family. They like to live around each other and go through much trouble finding houses
nearby. The social isolation from his family may be the stressor in Mr. C’s life leading to possible
depression, anxiety, and subsequent alcohol abuse.
CHAPTER 22: ANSWER KEY TO TEXT CASE STUDIES
Brief Patient History
Mrs. S is a 70-year-old woman with a long history of chronic back pain. She has been taking nonsteroidal
anti-inflammatory drugs (NSAIDs) for several years. She was recently started on warfarin for atrial
fibrillation.
Clinical Assessment
Mrs. S is admitted to the intensive care unit vomiting bright red blood. She is pale and diaphoretic, and
complains of epigastric pain.
Diagnostic Procedures
Blood pressure (BP), 70/40; heart rate (HR), 130 (sinus tachycardia); respiratory rate (RR), 30;
temperature (T), 101.3° F; urine output, 15 mL/hr; hemoglobin, 9 g/dL; international normalized ratio
(INR), 5.3.
Medical Diagnosis
Upper gastrointestinal bleed is diagnosed.
1. What major outcomes do you expect to achieve for this patient?
Answer: The major outcomes expected for Mrs. S include hemodynamic stability and hemostasis.
2. What problems or risks must be managed to achieve these outcomes?
Answer: Maintenance of tissue perfusion, volume resuscitation, and airway protection must be
managed.
3. What interventions must be initiated to monitor, prevent, manage, or eliminate the problems
and risks identified?
Answer: Mrs. S’s vital signs should be monitored. The bleeding source should be identified and
arrested. Laboratory values should be assessed, and blood product replacement should be
administered.
4. What interventions should be initiated to promote optimal functioning, safety, and well-being
of the patient?
Answer: Adherence to policy on blood product administration. Prompt recognition of transfusion
reactions and assessment of complications (e.g., rebleeding, aspiration).
5. What possible learning needs would you anticipate for this patient?
Answer: Mrs. S should be educated on the effect of NSAID use on the GI tract, monitoring of
anticoagulation, and an action plan in the event of further bleeding.
6. What cultural and age-related factors might have a bearing on the patient’s plan of care?
Answer: Mrs. S may have difficulty complying with a treatment plan due to potential memory
impairment, financial issues, and transportation limitations.