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Update the supporting evidence for the assessment problems and include a plan and rationale for EACH problem in the plan. Using the Global AKI Guidelines
Align each problem with each plan properly, keeping it very organized.
Use the “Denise Fields Case” as an example for organization.
Name: Denise Fields |
|
DOB: 5/9/1985 |
Date: 11/2 0 /23 |
||||||||||||||
Chief Compliant
“I’m here to follow up on the results of my labs”
History of Present Illness
A 38-year-old woman with type 2 diabetes mellitus (T2DM), hypertension (HTN), and dyslipidemia returns to her primary care physician (PCP) for a follow-up visit. At her routine physical examination 3 months ago, her annual nephropathy screening revealed a urine albumin-to-creatinine ratio (UACR) of 659 mg/g, which was elevated from the previous year’s screening that showed a mildly increased UACR of 145 mg/g and an SCr of 1.2 m
g/dL
. A second spot urine test from 1 week ago showed a persistently elevated UACR of
673
mg/g. She has returned to the office today to review her lab results and presents with no complaints. She brought with her a list of her medications and self-monitoring blood glucose readings.
Past Medical History
Medical Conditions: T2DM x 8 years, HTN x 6 years, Dyslipidemia x 5 years, seasonal allergies
Medications
Metformin 1000 mg PO twice daily
Semaglutide 0.5 mg mh injected subcutaneously once weekly
Hydrochlorothiazide 25 mg PO once daily
Atorvastatin 20 mg PO once daily
Mometasone 100 mcg two sprays in each nostril once daily prn allergies
Cetirizine 10 mg PO once daily prn allergies
Naproxen 220 mg PO twice daily prn headaches
Multivitamin PO once daily
Allergies
Seasonal: grass and pollen
Drug: NKDA
Family History
Mother: alive at age 62, has HTN and dyslipidemia
Father: passed at age 50 secondary to myocardial infarctions, had T2DM and CVD
Brother: alive at age 31, has T2DM
Social History
Education: high school graduate
Employment status: full time administrative assistant
Marital Status: married to husband, no children
Smoking Status: current 1 PPD smoker, decreased from last year (2 PPD)
Illicit Drugs: denies
ETOH: occasional consumption on weekends or when out with friends (1-2 beverages/week)
Review of Systems
Eyes: no vision changes
Cardiovascular: no chest pain or palpitations
Respiratory: no shortness of breath
Gastrointestinal: no polydipsia or polyphagia
Genitourinary: no polyuria
Musculoskeletal: no edema
Neurological: occasional headaches, generally associated with menstruation, no dizziness, fatigue, or sensory loss
Physical Examination
Constitutional: no acute distress
Neck/lymph nodes: supple without adenopathy or thyromegaly
HEENT: PEERLA, EOMI, negative for diabetic retinopathy; no retinal edema or vitreous hemorrhage; TMs intact; oral mucosa moist with no lesions
Cardiovascular: heart sounds normal, no murmurs, no bruits
Respiratory: clear, breath sounds normal
Gastrointestinal: soft NT/ND
Genitourinary: rectal exam deferred; recent PAP smear negative
Musculoskeletal: no CCE, normal ROM
Neurological: A&O x 3, CNs intact, normal DTRs
Skin: warm, dry, no rashes
Vitals 1
Height: 5 ft. 6 in.
Weight: 191 lbs.
BMI: 30.8
Systolic1: 148
Diastolic1: 84
Systolic2: 146
Diastolic2: 82
Pulse: 82
Resp:18
Temp: 37.5C
O2SAT: 98
%
Lab Reports (collected 1 week ago)
BMP LAB REPORT
Test Name |
Patient Results |
Reference Range |
Unit |
||||||||||||||||||||||||||||||||||||
SODIUM |
140 |
135 – 145 |
MEQ/L |
||||||||||||||||||||||||||||||||||||
POTASSIUM |
3.9 |
3.5 – 5 |
|||||||||||||||||||||||||||||||||||||
CHLORIDE |
107 |
98 – 106 |
|||||||||||||||||||||||||||||||||||||
CO2 |
26 |
22 -28 |
|||||||||||||||||||||||||||||||||||||
BUN |
29 |
8 – 20 |
M G/DL |
||||||||||||||||||||||||||||||||||||
CREATININE |
1.6 |
0.6 – 1.2 |
|||||||||||||||||||||||||||||||||||||
GLUCOSE |
196 |
65 – 99 |
|||||||||||||||||||||||||||||||||||||
CALCIUM |
9.4 |
8.6 – 1 0.2 |
|||||||||||||||||||||||||||||||||||||
PHOSPHORUS |
2.7 |
2.8 – 4.5 |
ESTIMATED GLOMERULAR FILTRATION RATE LAB REPORT
eGFR |
46.4 |
> 90 |
mL/min/1.73m2 |
CBC LAB REPORT
WBC |
9,500 |
4,000-10,000 |
cells/μL |
||
HGB |
12.2 |
12-17 |
g/dL | ||
HCT |
36.1% |
36-51 |
% | ||
MVC |
79 |
79-97 |
fL |
||
PLATELETS |
148,000 |
150,000-400,000 |
HbA1C LAB REPORT
HBA1C |
8.2 |
<5.7 |
PREGNANCY TEST LAB REPORT
HCG, qualitative |
NEGATIVE |
LIPID PANEL LAB REPORT
TOTAL CHOLESTEROL |
212 |
100 – 199 |
|
LDL, DIRECT |
149 |
0 – 99 |
|
HDL |
42 |
>39 |
|
TRIGLYCERIDES |
0 – 149 |
UA LAB REPORT
pH |
5.2 |
5 – 7.5 |
||
SPECIFIC GRAVITY |
1.020 |
1.001-1.029 |
||
URINE COLOR |
YELLOW |
|||
APPEARANCE |
CLEAR |
|||
PROTEIN |
325 |
< 20 |
mg/dL |
|
1+ GLUCOSE |
||||
KETONES |
||||
BLOOD |
||||
LEUKOCYTE ESTERASE |
||||
NITRITE |
||||
BILIRUBIN |
||||
UROBILINOGEN |
0.2 |
0.2 – 1 |
||
3-4 |
0 – 5 |
hpf |
||
RBC |
0 |
0 – 2 |
||
EPITHELIAL CELLS |
0 – 10 |
|||
CASTS |
NONE SEEN |
|||
BACTERIA |
MICRO
ALBUMIN
TO CREATINE RATIO LAB REPORT
MACR |
673 |
< 30 |
MG/G |
URIC ACID
LAB REPORT
URIC ACID |
6.2 |
2.3 – 7 |
ALBUMIN LAB REPORT
ALBUMIN |
3.4 |
3.5 – 5.5 |
G/DL |
Assessment
1. CKD with albuminuria (G3bA3) with inappropriate medication dosing
Supporting Evidence:
Subjective: patient does not report any complaints
Objective: worsening of SCr to 1.6 from 1.2 a year ago, eGFR of 42 mL/min (stage 3 CKD), MACR/UACR 673 up from 659 3 months ago and 145 1 year ago, CrCl = 53 mL/min
(ActualBW = 87 kg, IBW = 59.3 kg, AdjBW = 70.4 kg)
Non-pharmacologic options:
A. remove nephrotoxic agents
B. Dietary recommendations
– diet high in vegetables, fruit, whole grain, fiber, plant based proteins, unsaturated fats and nuts; low in processed meats, refined carbohydrates, and sweetened beverages
– dietary protein should be 0.8g/kg daily
– restrict sodium to < 2000 mg/day
C. Weight reduction
D. Physical exercise
E. Smoking cessation
Pharmacologic options:
A. Blood pressure management: the patient is currently above goal of < 130/80 on HCTZ therapy
Hydrochlorothiazide (current therapy)
Pros: currently tolerating therapy, efficacy with CrCl > 25-30 mL/min, first line therapy for HTN
Cons: electrolyte disturbances
ACE inhibitor (lisinopril)
Pros: slows the progression of kidney disease, first line in patients with CKD and diabetes with albuminuria
Cons: may increase SCr if not stable (AKI risk), cough, hyperkalemia, angioedema risk
ARB (losartan)
Pros: slows the progression of kidney disease, first line in patients with CKD and diabetes with albuminuria
Cons: may increase SCr if not stable (AKI risk), hyperkalemia, angioedema risk
CCB (amlodipine)
Pros: recommended first line therapy for most patients, no monitoring required, well tolerated
Cons: risk of edema (may be issue in patient with volume regulation issues)
B. Glycemic management: the patient is above A1c goal of 8.2% with metformin and Ozempic
Metformin
Pros: first line therapy for management of T2DM, oral medication, well tolerated
Cons: GI upset common, lactic acidosis, renal dose adjusted
GLP-1 RA (semaglutide/Ozepmic)
Pros: recommended after metformin and SGLT2 in patients with CKD, weight loss
Cons: GI adverse effects, injectable, risk of pancreatitis
SGLT-2 inhibitor
Pros: recommended first-line therapy for patient with CKD and diabetes over GLP1-RA, slows the progression of kidney disease, may lower BP
Cons: electrolyte disturbances, increased urination, risk of infection, require hydration
Insulin
Pros: safe in patients with CKD, but not recommended in patients until non-insulin therapy has been trialed or optimized if A1c < 10%
Cons: injectable, weight gain
C. Smoking cessation: patient willingness to quit was not assessed, but patient self-decreased smoking to 1 PPD
Dual NRT (Patch + gum or lozenge)
Pros: first line therapy, easy to use, dual target approach
Cons: should be paired with behavioral therapy, patch can cause skin irritation
Varenicline
Pros: first line therapy, flexible quit date strategy, oral therapy
Cons: should be paired with behavioral therapy, vivid dreams, psychiatric considerations, renal dose adjustment in severe kidney patient (not this patient)
D. Dyslipidemia management: patients LDL is 149 mg/dL on moderate intensity statin therapy and lifetime ASCVD risk score is 50%
Statins (atorvastatin)
Pros: first line medication of choice for all patients
Cons: myalgias/muscle weakness, rare rhabdomyolysis
E. Inappropriate medications/dosing: medication dosing should be continually assessed in patients with CKD and nephrotoxic agents should be avoided
Naproxen
– NSAID therapy is nephrotoxic and is known to worsen kidney impairment and increase the risk of AKI. It should be avoided in all patients with CKD
Metformin
– metformin should be renal dose adjusted based on eGFR due to risk of accumulation in kidney impairment increasing the risks of adverse effects including GI upset and lactic acidosis
– based on this patients eGFR the recommended daily dose is 1000mg/day
Plan
1. CKD with albuminuria (G3bA3) with inappropriate medication dosing
Goals: management of CKD is focused on the management of risk factors for progressive kidney disease: obesity, elevated BP (goal BP < 130/80), hyperglycemia (goal A1c < 7%), smoking, dyslipidemia, nephrotoxic medications
Nonpharmacologic Recommendation:
A. remove nephrotoxic agents
B. Dietary recommendations
– diet high in vegetables, fruit, whole grain, fiber, plant based proteins, unsaturated fats and nuts; low in processed meats, refined carbohydrates, and sweetened beverages
– dietary protein should be 0.8g/kg daily
– restrict sodium to < 2000 mg/day
C. Weight reduction
D. Physical exercise
E. assess willingness to quit smoking and discuss smoking cessation options
Pharmacologic Recommendation:
A. initiate lisinopril 5 mg by mouth once daily and continue hydrochlorothiazide 25 mg by mouth once daily
B. initiate canagliflozin 100 mg by mouth daily, decrease metformin to 500 mg by mouth twice daily, and continue semaglutide 0.5 mg injected subQ once weekly
C. increase atorvastatin to 40 mg by mouth once daily
D. discontinue naproxen 220 mg twice daily PRN and initiate acetaminophen 500 mg 1-2 tablets every 6 hours prn
E. continue all other medications as prescribed
Rationale:
A. an ACE inhibitor or ARB would be appropriate for BP lowering renal protection in the setting of CKD with albuminuria. Hydrochlorothiazide should also be continued because her BP is well above goal and patient likely needs combination therapy. Dose of lisinopril should be titrated slowly to a max of 40 mg/day
B. SGLT2 inhibitor therapy should be prioritized in combination with metformin in patients with diabetes and CKD over GLP-1RA therapy. SGTL2 inhibitor therapy may also reduce the patients BP. Metformin dose must be reduced due to renal impairment to a max of 1000mg/day. May consider increasing semaglutide to 1 mg at this time but with other changes today, it might be best to wait for follow up
C. patient has a high risk of lifetime ASCVD and many risk factors for CV disease. The patient is currently on moderate intensity statin therapy and LDL is 149 mg/dL. The patient would benefit from an increase to high intensity therapy and my benefit from targeting a max dose of atorvastatin 80 mg/day
D. naproxen is nephrotoxic and should be avoided, if the patient has not failed acetaminophen this would be an appropriate switch, if there is inadequate relief the patient should follow up with PCP for further assessment
E. patients current medications are dose appropriately considering the patients renal function and do not have disease interactions to be concerned about
Toxicity Monitoring:
· ACEi/ARB: patients’ potassium is 3.9 mEq/L and SCr 1.6 both can be increased with the initiation of therapy
· BMP in 7-10 days
· SGLT-2: transient increase in eGFR, especially in combination with ACE/ARB initiation; risk of electrolyte abnormalities
· BMP in 7-10 days
Therapeutic Efficacy Monitoring:
· CKD progression: monitor renal function and albuminuria
· BMP and MACR every 3-6 months
· HTN
· monitor BP at each encounter and at home daily
· T2DM
· A1c every 3 month until at goal x 2 then every 6 months
· SMBG daily
· Dyslipidemia: monitor for improvement in lipid panel
· FLP in 4-8 weeks
Patient Education:
· You have been diagnosed with a condition called chronic kidney disease or CKD. This can happen because of long-term uncontrolled diabetes, high blood pressure, certain medications, and other factors. Having CKD means that your kidneys are not able to filter the waste in your body as well anymore. Some medications will need to be changed to prevent build up or further damage to your kidneys. Our goal is preventing the further progression of the kidney disease and lower the risk of further complications. We will need to closely monitor your kidney function and labs moving forward to identify any progression early. It is important to consult your provide before taking any new medications since they may cause further damage to your kidneys.
· Stop taking naproxen or other NSAIDS to prevent damage to your kidneys, instead take acetaminophen 500 mg 1-2 tablets every 6 hours as needed, do not take more than 4000 mg of acetaminophen per day. Contact your provider if your headaches are not relieved
· Your metformin dose will need to be reduced since your kidney aren’t able to clear the medication as well anymore, which increases your risk of side effects with the medication.
· Canagliflozin is a new medication which can help lower you blood sugar and blood pressure. This medication also helps prevent the worsening of your kidney function. it may cause you to go to the bathroom more often and should be taken in the morning. It is important to stay hydrated while taking this medication because it increases the sugar in your urine which can increase your risk of urinary tract infections. Report any signs of infection to your doctor.
· Lisinopril is a new medication which will help lower your blood pressure and prevent progression of your kidney disease. This medication may cause an allergic reaction of the face which can lead to swelling of the face or tongue, if this occurs go directly to the ED. Let your provider know if you develop a dry cough on this medication and if you plan to become pregnant
Follow up:
Follow up in 1 week to repeat labs and then every 3 months.
page 1 of 1
page 1 of 1
1.
2.
3.
4.
5.
6.
Schwinghammer’s Pharmacotherapy Casebook: A PatientFocused Approach, 12th Edition
Chapter 54: Acute Kidney Injury: There’s Nothing Cute About It Level II
Scott Bolesta
Instructors can request access to the Casebook Instructor’s Guide on AccessPharmacy. Email Customer Success
(customersuccess@mheducation.com) for more information.
LEARNING OBJECTIVES
After completing this case study, the reader should be able to:
Assess a patient with AKI using clinical and laboratory data.
Classify AKI in a patient.
Distinguish between AKI resulting from prerenal and that from intrinsic injury.
Recommend changes to the pharmacotherapeutic regimen of a patient with AKI.
Justify appropriate therapeutic interventions for a patient with AKI.
PATIENT PRESENTATION
Chief Complaint
“I feel really weak.”
HPI
A 72yearold man presents to the ED with complaints of severe weakness that started this morning and recent stomach pain for the past week. He was
feeling well until he developed stomach pain 1 week ago that worsened with meals. Two days ago, the pain worsened to the point where he avoided
eating, and last evening he felt more tired than usual and went to bed early. He had difficulty sleeping due to the pain, and since waking this morning
he has been in too much pain and too weak to perform his normal ADLs.
PMH
HTN × 30 years
CAD × 20 years
MI × 2 with most recent 2 months ago s/p PCI with drugeluting stent placement
s/p CABG 20 years ago
HFrEF × 4 years
OA × 5 year
FH
Father died of an acute MI at age 52; mother had diabetes mellitus and died of a stroke at the age of 65.
SH
Retired and living at home with his wife. Before retirement, the patient was employed as an accountant. No alcohol, no tobacco use.
Meds
Aspirin 81 mg PO daily
Amlodipine 10 mg PO once daily
Furosemide 40 mg PO once daily
Metoprolol succinate 50 mg PO once daily
Enalapril 20 mg PO once daily
Prasugrel 10 mg PO daily
Atorvastatin 80 mg PO daily
Naproxen 500 mg PO BID
All
NKA
ROS
In addition to weakness and stomach pain, the patient complains of feeling cold but denies chills or fever. No changes in vision. Denies SOB, CP, and
cough. Complains of feeling lightheaded. Has been having frequent loose black stools over the past 3 days and abdominal pain that has become severe
in the past 2 days. Has noted a decrease in the frequency of his urination over the past 24 hours. Denies musculoskeletal pain or cramping.
Physical Examination
Gen
Pale man who appears in moderate distress and generally weak and lethargic
VS
BP 89/43 mm Hg (77/32 mm Hg on standing), P 123 bpm, RR 25, T 36.1°C; Wt 171.6 lb (78 kg), Ht 5′9″ (175 cm)
Skin
Pale and cool with poor turgor
HEENT
PERRLA; EOMI; fundi normal; conjunctivae pale and dry; TMs intact; tongue and mouth dry
Neck/Lymph Nodes
No JVD or HJR; no lymphadenopathy or thyromegaly
Lungs
No crackles or rhonchi
CV
Tachycardic with regular rhythm; normal S1, S2; no S3; faint S4; no MRG
Abd
Rigid with guarding, epigastric tenderness, ND; no HSM; hyperactive BS
Genit/Rect
Stool heme (+); slightly enlarged prostate
MS/Ext
Weak pulses; no peripheral edema; mild swelling of MCP joints of both hands
Neuro
A&O × 3; CNs intact; DTRs 2+; Babinski (–)
Labs
Na 132 mEq/L Ca 8.6 mg/dL
K 5.6 mEq/L Mg 2.1 mg/dL
Cl 97 mEq/L Phos 4.3 mg/dL
CO2 22 mEq/L WBC 8.6 × 103/mm3
BUN 53 mg/dL Hgb 7.6 g/dL
SCr 1.8 mg/dL Hct 22.5%
Glu 123 mg/dL Plt 96 × 103/mm3
Assessment
Admit to hospital for evaluation and management of dehydration, evaluation for acute GI bleed, and potential acute kidney injury.
Clinical Course
On admission, the patient was resuscitated aggressively with balanced crystalloids given IV and multiple transfusions (4 units of PRBCs). His home
medications were held, he was started on a continuous IV pantoprazole infusion of 8 mg/hr, and he underwent an emergent EGD. During endoscopy, a
large ulcer in the gastric antrum was found with an exposed spurting artery. Endoscopic therapy was unsuccessful, and the patient was taken to the OR
for surgical intervention. He was hypotensive in the OR (BP 70 mm Hg systolic on average) and was started on a norepinephrine infusion to maintain a
stable BP. Postoperatively, he remained on mechanical ventilation, and his urine output averaged 35 mL/hr over the first 12 postoperative hours
despite continued IV hydration and repeated transfusions in the OR. He also remained on norepinephrine for a continued low BP. On the morning of
postoperative day 1, his labs were as follows:
Na 134 mEq/L Ca 8.2 mg/dL
K 5.4 mEq/L Mg 2.2 mg/dL
Cl 111 mEq/L Phos 4.7 mg/dL
CO2 19 mEq/L WBC 14.6 × 103/mm3
BUN 49 mg/dL Hgb 10.3 g/dL
SCr 2.5 mg/dL Hct 29.8%
Glu 145 mg/dL Plt 112 × 103/mm3
Urinalysis also showed muddy brown casts, urine sodium of 72 mEq/L, and specific gravity of 1.004. The patient remained on mechanical ventilation
and norepinephrine, his urine output had not improved, and his chest radiograph showed diffuse bilateral pulmonary edema with a decrease in O2
saturation to 86%. An echocardiogram revealed hypokinesis of the anterior portion of the left ventricle and an EF of 25%. The patient was started on
dobutamine, and an internal jugular vein catheter was inserted and CVVHDF was begun.
Assessment
A 72yearold man with an acute UGI bleed, AKI, and volume overload heart failure.
QUESTIONS
Collect Information
1.a. What subjective and objective information indicates the presence of AKI postoperatively?
1.b. What additional information is needed to fully assess this patient’s AKI postoperatively?
Assess the Information
2.a. Assess the severity of AKI based on the subjective and objective information available.
2.b. Create a list of the patient’s drug therapy problems and prioritize them. Include assessment of medication appropriateness, effectiveness, safety,
and patient adherence.
Develop a Care Plan
3.a. What are the goals of pharmacotherapy for AKI in this case?
3.b. What nondrug therapies might be useful for this patient’s AKI?
3.c. What feasible pharmacotherapeutic options are available for treating AKI?
3.d. Create an individualized, patientcentered, teambased care plan to optimize medication therapy for the AKI and other drug therapy problems.
Include specific drugs, dosage forms, doses, schedules, and durations of therapy.
Implement the Care Plan
4.a. What information should be provided to the patient to enhance adherence, ensure successful therapy, and minimize adverse effects?
4.b. Describe how care should be coordinated with other healthcare providers.
FollowUp: Monitor and Evaluate
5 . Explain how to monitor and evaluate the care plan for medication appropriateness, effectiveness, safety, and patient adherence by using clinical and
laboratory data, patient feedback, and other information.
CLINICAL COURSE
On postoperative day 5, his pulmonary edema had resolved, he had been weaned off norepinephrine and dobutamine, the dialysis catheter was
removed, and he was extubated. His subsequent hospital course was uneventful, and his kidney function gradually improved.
SELFSTUDY ASSIGNMENTS
1 . Evaluate the evidence regarding the effectiveness of intravenous 0.9% sodium chloride compared to balanced crystalloids (eg, Plasmalyte, Ringer’s
lactate) in volume resuscitation for outcomes related to kidney function.
2 . Write a brief paper that discusses the utilization of intravenous sodium bicarbonate in the setting of AKI in patients who present with shock.
CLINICAL PEARL
Most laboratory markers of kidney function (eg, serum creatinine) in patients with AKI usually lag behind the true change in GFR, often by a day or
more. Therefore, adjustment of drug therapy dosing in these patients can be challenging, and often trends in urine output over the previous hours are
used to anticipate the need to make dose adjustments.
REFERENCES
Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO clinical practice guideline for acute kidney injury.
Kidney Inter Suppl. 2012;2:1–138.
Semler MW, Self WH, Wanderer JP, et al. Balanced crystalloids versus saline in critically ill adults. N Engl J Med. 2018;378(9):829–839. [PubMed:
29485925]
Prowle JR, Kirwan CJ, Bellomo R. Fluid management for the prevention and attenuation of acute kidney injury. Nat Rev Nephrol. 2014;10:37–47.
[PubMed: 24217464]
Palevsky PM. Renal replacement therapy in acute kidney injury. Adv Chronic Kidney Dis. 2013;20:76–84. [PubMed: 23265599]
Ejaz AA, Mohandas R. Are diuretics harmful in the management of acute kidney injury? Curr Opin Nephrol Hypertens. 2014;23:155–160. [PubMed:
24389731]
Kellum JA, Lameire N. Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (part 1). Crit Care. 2013;17:204. [PubMed:
23394211]
Texas Southern University Sch of Pharmacy
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1.
2.
3.
4.
5.
6.
Schwinghammer’s Pharmacotherapy Casebook: A PatientFocused Approach, 12th Edition
Chapter 54: Acute Kidney Injury: There’s Nothing Cute About It Level II
Scott Bolesta
Instructors can request access to the Casebook Instructor’s Guide on AccessPharmacy. Email Customer Success
(customersuccess@mheducation.com) for more information.
LEARNING OBJECTIVES
After completing this case study, the reader should be able to:
Assess a patient with AKI using clinical and laboratory data.
Classify AKI in a patient.
Distinguish between AKI resulting from prerenal and that from intrinsic injury.
Recommend changes to the pharmacotherapeutic regimen of a patient with AKI.
Justify appropriate therapeutic interventions for a patient with AKI.
PATIENT PRESENTATION
Chief Complaint
“I feel really weak.”
HPI
A 72yearold man presents to the ED with complaints of severe weakness that started this morning and recent stomach pain for the past week. He was
feeling well until he developed stomach pain 1 week ago that worsened with meals. Two days ago, the pain worsened to the point where he avoided
eating, and last evening he felt more tired than usual and went to bed early. He had difficulty sleeping due to the pain, and since waking this morning
he has been in too much pain and too weak to perform his normal ADLs.
PMH
HTN × 30 years
CAD × 20 years
MI × 2 with most recent 2 months ago s/p PCI with drugeluting stent placement
s/p CABG 20 years ago
HFrEF × 4 years
OA × 5 year
FH
Father died of an acute MI at age 52; mother had diabetes mellitus and died of a stroke at the age of 65.
SH
Retired and living at home with his wife. Before retirement, the patient was employed as an accountant. No alcohol, no tobacco use.
Meds
Aspirin 81 mg PO daily
Amlodipine 10 mg PO once daily
Furosemide 40 mg PO once daily
Metoprolol succinate 50 mg PO once daily
Enalapril 20 mg PO once daily
Prasugrel 10 mg PO daily
Atorvastatin 80 mg PO daily
Naproxen 500 mg PO BID
All
NKA
ROS
In addition to weakness and stomach pain, the patient complains of feeling cold but denies chills or fever. No changes in vision. Denies SOB, CP, and
cough. Complains of feeling lightheaded. Has been having frequent loose black stools over the past 3 days and abdominal pain that has become severe
in the past 2 days. Has noted a decrease in the frequency of his urination over the past 24 hours. Denies musculoskeletal pain or cramping.
Physical Examination
Gen
Pale man who appears in moderate distress and generally weak and lethargic
VS
BP 89/43 mm Hg (77/32 mm Hg on standing), P 123 bpm, RR 25, T 36.1°C; Wt 171.6 lb (78 kg), Ht 5′9″ (175 cm)
Skin
Pale and cool with poor turgor
HEENT
PERRLA; EOMI; fundi normal; conjunctivae pale and dry; TMs intact; tongue and mouth dry
Neck/Lymph Nodes
No JVD or HJR; no lymphadenopathy or thyromegaly
Lungs
No crackles or rhonchi
CV
Tachycardic with regular rhythm; normal S1, S2; no S3; faint S4; no MRG
Abd
Rigid with guarding, epigastric tenderness, ND; no HSM; hyperactive BS
Genit/Rect
Stool heme (+); slightly enlarged prostate
MS/Ext
Weak pulses; no peripheral edema; mild swelling of MCP joints of both hands
Neuro
A&O × 3; CNs intact; DTRs 2+; Babinski (–)
Labs
Na 132 mEq/L Ca 8.6 mg/dL
K 5.6 mEq/L Mg 2.1 mg/dL
Cl 97 mEq/L Phos 4.3 mg/dL
CO2 22 mEq/L WBC 8.6 × 103/mm3
BUN 53 mg/dL Hgb 7.6 g/dL
SCr 1.8 mg/dL Hct 22.5%
Glu 123 mg/dL Plt 96 × 103/mm3
Assessment
Admit to hospital for evaluation and management of dehydration, evaluation for acute GI bleed, and potential acute kidney injury.
Clinical Course
On admission, the patient was resuscitated aggressively with balanced crystalloids given IV and multiple transfusions (4 units of PRBCs). His home
medications were held, he was started on a continuous IV pantoprazole infusion of 8 mg/hr, and he underwent an emergent EGD. During endoscopy, a
large ulcer in the gastric antrum was found with an exposed spurting artery. Endoscopic therapy was unsuccessful, and the patient was taken to the OR
for surgical intervention. He was hypotensive in the OR (BP 70 mm Hg systolic on average) and was started on a norepinephrine infusion to maintain a
stable BP. Postoperatively, he remained on mechanical ventilation, and his urine output averaged 35 mL/hr over the first 12 postoperative hours
despite continued IV hydration and repeated transfusions in the OR. He also remained on norepinephrine for a continued low BP. On the morning of
postoperative day 1, his labs were as follows:
Na 134 mEq/L Ca 8.2 mg/dL
K 5.4 mEq/L Mg 2.2 mg/dL
Cl 111 mEq/L Phos 4.7 mg/dL
CO2 19 mEq/L WBC 14.6 × 103/mm3
BUN 49 mg/dL Hgb 10.3 g/dL
SCr 2.5 mg/dL Hct 29.8%
Glu 145 mg/dL Plt 112 × 103/mm3
Urinalysis also showed muddy brown casts, urine sodium of 72 mEq/L, and specific gravity of 1.004. The patient remained on mechanical ventilation
and norepinephrine, his urine output had not improved, and his chest radiograph showed diffuse bilateral pulmonary edema with a decrease in O2
saturation to 86%. An echocardiogram revealed hypokinesis of the anterior portion of the left ventricle and an EF of 25%. The patient was started on
dobutamine, and an internal jugular vein catheter was inserted and CVVHDF was begun.
Assessment
A 72yearold man with an acute UGI bleed, AKI, and volume overload heart failure.
QUESTIONS
Collect Information
1.a. What subjective and objective information indicates the presence of AKI postoperatively?
1.b. What additional information is needed to fully assess this patient’s AKI postoperatively?
Assess the Information
2.a. Assess the severity of AKI based on the subjective and objective information available.
2.b. Create a list of the patient’s drug therapy problems and prioritize them. Include assessment of medication appropriateness, effectiveness, safety,
and patient adherence.
Develop a Care Plan
3.a. What are the goals of pharmacotherapy for AKI in this case?
3.b. What nondrug therapies might be useful for this patient’s AKI?
3.c. What feasible pharmacotherapeutic options are available for treating AKI?
3.d. Create an individualized, patientcentered, teambased care plan to optimize medication therapy for the AKI and other drug therapy problems.
Include specific drugs, dosage forms, doses, schedules, and durations of therapy.
Implement the Care Plan
4.a. What information should be provided to the patient to enhance adherence, ensure successful therapy, and minimize adverse effects?
4.b. Describe how care should be coordinated with other healthcare providers.
FollowUp: Monitor and Evaluate
5 . Explain how to monitor and evaluate the care plan for medication appropriateness, effectiveness, safety, and patient adherence by using clinical and
laboratory data, patient feedback, and other information.
CLINICAL COURSE
On postoperative day 5, his pulmonary edema had resolved, he had been weaned off norepinephrine and dobutamine, the dialysis catheter was
removed, and he was extubated. His subsequent hospital course was uneventful, and his kidney function gradually improved.
SELFSTUDY ASSIGNMENTS
1 . Evaluate the evidence regarding the effectiveness of intravenous 0.9% sodium chloride compared to balanced crystalloids (eg, Plasmalyte, Ringer’s
lactate) in volume resuscitation for outcomes related to kidney function.
2 . Write a brief paper that discusses the utilization of intravenous sodium bicarbonate in the setting of AKI in patients who present with shock.
CLINICAL PEARL
Most laboratory markers of kidney function (eg, serum creatinine) in patients with AKI usually lag behind the true change in GFR, often by a day or
more. Therefore, adjustment of drug therapy dosing in these patients can be challenging, and often trends in urine output over the previous hours are
used to anticipate the need to make dose adjustments.
REFERENCES
Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO clinical practice guideline for acute kidney injury.
Kidney Inter Suppl. 2012;2:1–138.
Semler MW, Self WH, Wanderer JP, et al. Balanced crystalloids versus saline in critically ill adults. N Engl J Med. 2018;378(9):829–839. [PubMed:
29485925]
Prowle JR, Kirwan CJ, Bellomo R. Fluid management for the prevention and attenuation of acute kidney injury. Nat Rev Nephrol. 2014;10:37–47.
[PubMed: 24217464]
Palevsky PM. Renal replacement therapy in acute kidney injury. Adv Chronic Kidney Dis. 2013;20:76–84. [PubMed: 23265599]
Ejaz AA, Mohandas R. Are diuretics harmful in the management of acute kidney injury? Curr Opin Nephrol Hypertens. 2014;23:155–160. [PubMed:
24389731]
Kellum JA, Lameire N. Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (part 1). Crit Care. 2013;17:204. [PubMed:
23394211]
Texas Southern University Sch of Pharmacy
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Schwinghammer’s Pharmacotherapy Casebook: A PatientFocused Approach, 12th Edition
Chapter 54: Acute Kidney Injury: There’s Nothing Cute About It Level II
Scott Bolesta
Instructors can request access to the Casebook Instructor’s Guide on AccessPharmacy. Email Customer Success
(customersuccess@mheducation.com) for more information.
LEARNING OBJECTIVES
After completing this case study, the reader should be able to:
Assess a patient with AKI using clinical and laboratory data.
Classify AKI in a patient.
Distinguish between AKI resulting from prerenal and that from intrinsic injury.
Recommend changes to the pharmacotherapeutic regimen of a patient with AKI.
Justify appropriate therapeutic interventions for a patient with AKI.
PATIENT PRESENTATION
Chief Complaint
“I feel really weak.”
HPI
A 72yearold man presents to the ED with complaints of severe weakness that started this morning and recent stomach pain for the past week. He was
feeling well until he developed stomach pain 1 week ago that worsened with meals. Two days ago, the pain worsened to the point where he avoided
eating, and last evening he felt more tired than usual and went to bed early. He had difficulty sleeping due to the pain, and since waking this morning
he has been in too much pain and too weak to perform his normal ADLs.
PMH
HTN × 30 years
CAD × 20 years
MI × 2 with most recent 2 months ago s/p PCI with drugeluting stent placement
s/p CABG 20 years ago
HFrEF × 4 years
OA × 5 year
FH
Father died of an acute MI at age 52; mother had diabetes mellitus and died of a stroke at the age of 65.
SH
Retired and living at home with his wife. Before retirement, the patient was employed as an accountant. No alcohol, no tobacco use.
Meds
Aspirin 81 mg PO daily
Amlodipine 10 mg PO once daily
Furosemide 40 mg PO once daily
Metoprolol succinate 50 mg PO once daily
Enalapril 20 mg PO once daily
Prasugrel 10 mg PO daily
Atorvastatin 80 mg PO daily
Naproxen 500 mg PO BID
All
NKA
ROS
In addition to weakness and stomach pain, the patient complains of feeling cold but denies chills or fever. No changes in vision. Denies SOB, CP, and
cough. Complains of feeling lightheaded. Has been having frequent loose black stools over the past 3 days and abdominal pain that has become severe
in the past 2 days. Has noted a decrease in the frequency of his urination over the past 24 hours. Denies musculoskeletal pain or cramping.
Physical Examination
Gen
Pale man who appears in moderate distress and generally weak and lethargic
VS
BP 89/43 mm Hg (77/32 mm Hg on standing), P 123 bpm, RR 25, T 36.1°C; Wt 171.6 lb (78 kg), Ht 5′9″ (175 cm)
Skin
Pale and cool with poor turgor
HEENT
PERRLA; EOMI; fundi normal; conjunctivae pale and dry; TMs intact; tongue and mouth dry
Neck/Lymph Nodes
No JVD or HJR; no lymphadenopathy or thyromegaly
Lungs
No crackles or rhonchi
CV
Tachycardic with regular rhythm; normal S1, S2; no S3; faint S4; no MRG
Abd
Rigid with guarding, epigastric tenderness, ND; no HSM; hyperactive BS
Genit/Rect
Stool heme (+); slightly enlarged prostate
MS/Ext
Weak pulses; no peripheral edema; mild swelling of MCP joints of both hands
Neuro
A&O × 3; CNs intact; DTRs 2+; Babinski (–)
Labs
Na 132 mEq/L Ca 8.6 mg/dL
K 5.6 mEq/L Mg 2.1 mg/dL
Cl 97 mEq/L Phos 4.3 mg/dL
CO2 22 mEq/L WBC 8.6 × 103/mm3
BUN 53 mg/dL Hgb 7.6 g/dL
SCr 1.8 mg/dL Hct 22.5%
Glu 123 mg/dL Plt 96 × 103/mm3
Assessment
Admit to hospital for evaluation and management of dehydration, evaluation for acute GI bleed, and potential acute kidney injury.
Clinical Course
On admission, the patient was resuscitated aggressively with balanced crystalloids given IV and multiple transfusions (4 units of PRBCs). His home
medications were held, he was started on a continuous IV pantoprazole infusion of 8 mg/hr, and he underwent an emergent EGD. During endoscopy, a
large ulcer in the gastric antrum was found with an exposed spurting artery. Endoscopic therapy was unsuccessful, and the patient was taken to the OR
for surgical intervention. He was hypotensive in the OR (BP 70 mm Hg systolic on average) and was started on a norepinephrine infusion to maintain a
stable BP. Postoperatively, he remained on mechanical ventilation, and his urine output averaged 35 mL/hr over the first 12 postoperative hours
despite continued IV hydration and repeated transfusions in the OR. He also remained on norepinephrine for a continued low BP. On the morning of
postoperative day 1, his labs were as follows:
Na 134 mEq/L Ca 8.2 mg/dL
K 5.4 mEq/L Mg 2.2 mg/dL
Cl 111 mEq/L Phos 4.7 mg/dL
CO2 19 mEq/L WBC 14.6 × 103/mm3
BUN 49 mg/dL Hgb 10.3 g/dL
SCr 2.5 mg/dL Hct 29.8%
Glu 145 mg/dL Plt 112 × 103/mm3
Urinalysis also showed muddy brown casts, urine sodium of 72 mEq/L, and specific gravity of 1.004. The patient remained on mechanical ventilation
and norepinephrine, his urine output had not improved, and his chest radiograph showed diffuse bilateral pulmonary edema with a decrease in O2
saturation to 86%. An echocardiogram revealed hypokinesis of the anterior portion of the left ventricle and an EF of 25%. The patient was started on
dobutamine, and an internal jugular vein catheter was inserted and CVVHDF was begun.
Assessment
A 72yearold man with an acute UGI bleed, AKI, and volume overload heart failure.
QUESTIONS
Collect Information
1.a. What subjective and objective information indicates the presence of AKI postoperatively?
1.b. What additional information is needed to fully assess this patient’s AKI postoperatively?
Assess the Information
2.a. Assess the severity of AKI based on the subjective and objective information available.
2.b. Create a list of the patient’s drug therapy problems and prioritize them. Include assessment of medication appropriateness, effectiveness, safety,
and patient adherence.
Develop a Care Plan
3.a. What are the goals of pharmacotherapy for AKI in this case?
3.b. What nondrug therapies might be useful for this patient’s AKI?
3.c. What feasible pharmacotherapeutic options are available for treating AKI?
3.d. Create an individualized, patientcentered, teambased care plan to optimize medication therapy for the AKI and other drug therapy problems.
Include specific drugs, dosage forms, doses, schedules, and durations of therapy.
Implement the Care Plan
4.a. What information should be provided to the patient to enhance adherence, ensure successful therapy, and minimize adverse effects?
4.b. Describe how care should be coordinated with other healthcare providers.
FollowUp: Monitor and Evaluate
5 . Explain how to monitor and evaluate the care plan for medication appropriateness, effectiveness, safety, and patient adherence by using clinical and
laboratory data, patient feedback, and other information.
CLINICAL COURSE
On postoperative day 5, his pulmonary edema had resolved, he had been weaned off norepinephrine and dobutamine, the dialysis catheter was
removed, and he was extubated. His subsequent hospital course was uneventful, and his kidney function gradually improved.
SELFSTUDY ASSIGNMENTS
1 . Evaluate the evidence regarding the effectiveness of intravenous 0.9% sodium chloride compared to balanced crystalloids (eg, Plasmalyte, Ringer’s
lactate) in volume resuscitation for outcomes related to kidney function.
2 . Write a brief paper that discusses the utilization of intravenous sodium bicarbonate in the setting of AKI in patients who present with shock.
CLINICAL PEARL
Most laboratory markers of kidney function (eg, serum creatinine) in patients with AKI usually lag behind the true change in GFR, often by a day or
more. Therefore, adjustment of drug therapy dosing in these patients can be challenging, and often trends in urine output over the previous hours are
used to anticipate the need to make dose adjustments.
REFERENCES
Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO clinical practice guideline for acute kidney injury.
Kidney Inter Suppl. 2012;2:1–138.
Semler MW, Self WH, Wanderer JP, et al. Balanced crystalloids versus saline in critically ill adults. N Engl J Med. 2018;378(9):829–839. [PubMed:
29485925]
Prowle JR, Kirwan CJ, Bellomo R. Fluid management for the prevention and attenuation of acute kidney injury. Nat Rev Nephrol. 2014;10:37–47.
[PubMed: 24217464]
Palevsky PM. Renal replacement therapy in acute kidney injury. Adv Chronic Kidney Dis. 2013;20:76–84. [PubMed: 23265599]
Ejaz AA, Mohandas R. Are diuretics harmful in the management of acute kidney injury? Curr Opin Nephrol Hypertens. 2014;23:155–160. [PubMed:
24389731]
Kellum JA, Lameire N. Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (part 1). Crit Care. 2013;17:204. [PubMed:
23394211]
Texas Southern University Sch of Pharmacy
Access Provided by:
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1.
2.
3.
4.
5.
6.
Schwinghammer’s Pharmacotherapy Casebook: A PatientFocused Approach, 12th Edition
Chapter 54: Acute Kidney Injury: There’s Nothing Cute About It Level II
Scott Bolesta
Instructors can request access to the Casebook Instructor’s Guide on AccessPharmacy. Email Customer Success
(customersuccess@mheducation.com) for more information.
LEARNING OBJECTIVES
After completing this case study, the reader should be able to:
Assess a patient with AKI using clinical and laboratory data.
Classify AKI in a patient.
Distinguish between AKI resulting from prerenal and that from intrinsic injury.
Recommend changes to the pharmacotherapeutic regimen of a patient with AKI.
Justify appropriate therapeutic interventions for a patient with AKI.
PATIENT PRESENTATION
Chief Complaint
“I feel really weak.”
HPI
A 72yearold man presents to the ED with complaints of severe weakness that started this morning and recent stomach pain for the past week. He was
feeling well until he developed stomach pain 1 week ago that worsened with meals. Two days ago, the pain worsened to the point where he avoided
eating, and last evening he felt more tired than usual and went to bed early. He had difficulty sleeping due to the pain, and since waking this morning
he has been in too much pain and too weak to perform his normal ADLs.
PMH
HTN × 30 years
CAD × 20 years
MI × 2 with most recent 2 months ago s/p PCI with drugeluting stent placement
s/p CABG 20 years ago
HFrEF × 4 years
OA × 5 year
FH
Father died of an acute MI at age 52; mother had diabetes mellitus and died of a stroke at the age of 65.
SH
Retired and living at home with his wife. Before retirement, the patient was employed as an accountant. No alcohol, no tobacco use.
Meds
Aspirin 81 mg PO daily
Amlodipine 10 mg PO once daily
Furosemide 40 mg PO once daily
Metoprolol succinate 50 mg PO once daily
Enalapril 20 mg PO once daily
Prasugrel 10 mg PO daily
Atorvastatin 80 mg PO daily
Naproxen 500 mg PO BID
All
NKA
ROS
In addition to weakness and stomach pain, the patient complains of feeling cold but denies chills or fever. No changes in vision. Denies SOB, CP, and
cough. Complains of feeling lightheaded. Has been having frequent loose black stools over the past 3 days and abdominal pain that has become severe
in the past 2 days. Has noted a decrease in the frequency of his urination over the past 24 hours. Denies musculoskeletal pain or cramping.
Physical Examination
Gen
Pale man who appears in moderate distress and generally weak and lethargic
VS
BP 89/43 mm Hg (77/32 mm Hg on standing), P 123 bpm, RR 25, T 36.1°C; Wt 171.6 lb (78 kg), Ht 5′9″ (175 cm)
Skin
Pale and cool with poor turgor
HEENT
PERRLA; EOMI; fundi normal; conjunctivae pale and dry; TMs intact; tongue and mouth dry
Neck/Lymph Nodes
No JVD or HJR; no lymphadenopathy or thyromegaly
Lungs
No crackles or rhonchi
CV
Tachycardic with regular rhythm; normal S1, S2; no S3; faint S4; no MRG
Abd
Rigid with guarding, epigastric tenderness, ND; no HSM; hyperactive BS
Genit/Rect
Stool heme (+); slightly enlarged prostate
MS/Ext
Weak pulses; no peripheral edema; mild swelling of MCP joints of both hands
Neuro
A&O × 3; CNs intact; DTRs 2+; Babinski (–)
Labs
Na 132 mEq/L Ca 8.6 mg/dL
K 5.6 mEq/L Mg 2.1 mg/dL
Cl 97 mEq/L Phos 4.3 mg/dL
CO2 22 mEq/L WBC 8.6 × 103/mm3
BUN 53 mg/dL Hgb 7.6 g/dL
SCr 1.8 mg/dL Hct 22.5%
Glu 123 mg/dL Plt 96 × 103/mm3
Assessment
Admit to hospital for evaluation and management of dehydration, evaluation for acute GI bleed, and potential acute kidney injury.
Clinical Course
On admission, the patient was resuscitated aggressively with balanced crystalloids given IV and multiple transfusions (4 units of PRBCs). His home
medications were held, he was started on a continuous IV pantoprazole infusion of 8 mg/hr, and he underwent an emergent EGD. During endoscopy, a
large ulcer in the gastric antrum was found with an exposed spurting artery. Endoscopic therapy was unsuccessful, and the patient was taken to the OR
for surgical intervention. He was hypotensive in the OR (BP 70 mm Hg systolic on average) and was started on a norepinephrine infusion to maintain a
stable BP. Postoperatively, he remained on mechanical ventilation, and his urine output averaged 35 mL/hr over the first 12 postoperative hours
despite continued IV hydration and repeated transfusions in the OR. He also remained on norepinephrine for a continued low BP. On the morning of
postoperative day 1, his labs were as follows:
Na 134 mEq/L Ca 8.2 mg/dL
K 5.4 mEq/L Mg 2.2 mg/dL
Cl 111 mEq/L Phos 4.7 mg/dL
CO2 19 mEq/L WBC 14.6 × 103/mm3
BUN 49 mg/dL Hgb 10.3 g/dL
SCr 2.5 mg/dL Hct 29.8%
Glu 145 mg/dL Plt 112 × 103/mm3
Urinalysis also showed muddy brown casts, urine sodium of 72 mEq/L, and specific gravity of 1.004. The patient remained on mechanical ventilation
and norepinephrine, his urine output had not improved, and his chest radiograph showed diffuse bilateral pulmonary edema with a decrease in O2
saturation to 86%. An echocardiogram revealed hypokinesis of the anterior portion of the left ventricle and an EF of 25%. The patient was started on
dobutamine, and an internal jugular vein catheter was inserted and CVVHDF was begun.
Assessment
A 72yearold man with an acute UGI bleed, AKI, and volume overload heart failure.
QUESTIONS
Collect Information
1.a. What subjective and objective information indicates the presence of AKI postoperatively?
1.b. What additional information is needed to fully assess this patient’s AKI postoperatively?
Assess the Information
2.a. Assess the severity of AKI based on the subjective and objective information available.
2.b. Create a list of the patient’s drug therapy problems and prioritize them. Include assessment of medication appropriateness, effectiveness, safety,
and patient adherence.
Develop a Care Plan
3.a. What are the goals of pharmacotherapy for AKI in this case?
3.b. What nondrug therapies might be useful for this patient’s AKI?
3.c. What feasible pharmacotherapeutic options are available for treating AKI?
3.d. Create an individualized, patientcentered, teambased care plan to optimize medication therapy for the AKI and other drug therapy problems.
Include specific drugs, dosage forms, doses, schedules, and durations of therapy.
Implement the Care Plan
4.a. What information should be provided to the patient to enhance adherence, ensure successful therapy, and minimize adverse effects?
4.b. Describe how care should be coordinated with other healthcare providers.
FollowUp: Monitor and Evaluate
5 . Explain how to monitor and evaluate the care plan for medication appropriateness, effectiveness, safety, and patient adherence by using clinical and
laboratory data, patient feedback, and other information.
CLINICAL COURSE
On postoperative day 5, his pulmonary edema had resolved, he had been weaned off norepinephrine and dobutamine, the dialysis catheter was
removed, and he was extubated. His subsequent hospital course was uneventful, and his kidney function gradually improved.
SELFSTUDY ASSIGNMENTS
1 . Evaluate the evidence regarding the effectiveness of intravenous 0.9% sodium chloride compared to balanced crystalloids (eg, Plasmalyte, Ringer’s
lactate) in volume resuscitation for outcomes related to kidney function.
2 . Write a brief paper that discusses the utilization of intravenous sodium bicarbonate in the setting of AKI in patients who present with shock.
CLINICAL PEARL
Most laboratory markers of kidney function (eg, serum creatinine) in patients with AKI usually lag behind the true change in GFR, often by a day or
more. Therefore, adjustment of drug therapy dosing in these patients can be challenging, and often trends in urine output over the previous hours are
used to anticipate the need to make dose adjustments.
REFERENCES
Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO clinical practice guideline for acute kidney injury.
Kidney Inter Suppl. 2012;2:1–138.
Semler MW, Self WH, Wanderer JP, et al. Balanced crystalloids versus saline in critically ill adults. N Engl J Med. 2018;378(9):829–839. [PubMed:
29485925]
Prowle JR, Kirwan CJ, Bellomo R. Fluid management for the prevention and attenuation of acute kidney injury. Nat Rev Nephrol. 2014;10:37–47.
[PubMed: 24217464]
Palevsky PM. Renal replacement therapy in acute kidney injury. Adv Chronic Kidney Dis. 2013;20:76–84. [PubMed: 23265599]
Ejaz AA, Mohandas R. Are diuretics harmful in the management of acute kidney injury? Curr Opin Nephrol Hypertens. 2014;23:155–160. [PubMed:
24389731]
Kellum JA, Lameire N. Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (part 1). Crit Care. 2013;17:204. [PubMed:
23394211]
Texas Southern University Sch of Pharmacy
Access Provided by:
Downloaded 2024731 12:10 P Your IP is 132.174.248.24
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3.
4.
5.
6.
Schwinghammer’s Pharmacotherapy Casebook: A PatientFocused Approach, 12th Edition
Chapter 54: Acute Kidney Injury: There’s Nothing Cute About It Level II
Scott Bolesta
Instructors can request access to the Casebook Instructor’s Guide on AccessPharmacy. Email Customer Success
(customersuccess@mheducation.com) for more information.
LEARNING OBJECTIVES
After completing this case study, the reader should be able to:
Assess a patient with AKI using clinical and laboratory data.
Classify AKI in a patient.
Distinguish between AKI resulting from prerenal and that from intrinsic injury.
Recommend changes to the pharmacotherapeutic regimen of a patient with AKI.
Justify appropriate therapeutic interventions for a patient with AKI.
PATIENT PRESENTATION
Chief Complaint
“I feel really weak.”
HPI
A 72yearold man presents to the ED with complaints of severe weakness that started this morning and recent stomach pain for the past week. He was
feeling well until he developed stomach pain 1 week ago that worsened with meals. Two days ago, the pain worsened to the point where he avoided
eating, and last evening he felt more tired than usual and went to bed early. He had difficulty sleeping due to the pain, and since waking this morning
he has been in too much pain and too weak to perform his normal ADLs.
PMH
HTN × 30 years
CAD × 20 years
MI × 2 with most recent 2 months ago s/p PCI with drugeluting stent placement
s/p CABG 20 years ago
HFrEF × 4 years
OA × 5 year
FH
Father died of an acute MI at age 52; mother had diabetes mellitus and died of a stroke at the age of 65.
SH
Retired and living at home with his wife. Before retirement, the patient was employed as an accountant. No alcohol, no tobacco use.
Meds
Aspirin 81 mg PO daily
Amlodipine 10 mg PO once daily
Furosemide 40 mg PO once daily
Metoprolol succinate 50 mg PO once daily
Enalapril 20 mg PO once daily
Prasugrel 10 mg PO daily
Atorvastatin 80 mg PO daily
Naproxen 500 mg PO BID
All
NKA
ROS
In addition to weakness and stomach pain, the patient complains of feeling cold but denies chills or fever. No changes in vision. Denies SOB, CP, and
cough. Complains of feeling lightheaded. Has been having frequent loose black stools over the past 3 days and abdominal pain that has become severe
in the past 2 days. Has noted a decrease in the frequency of his urination over the past 24 hours. Denies musculoskeletal pain or cramping.
Physical Examination
Gen
Pale man who appears in moderate distress and generally weak and lethargic
VS
BP 89/43 mm Hg (77/32 mm Hg on standing), P 123 bpm, RR 25, T 36.1°C; Wt 171.6 lb (78 kg), Ht 5′9″ (175 cm)
Skin
Pale and cool with poor turgor
HEENT
PERRLA; EOMI; fundi normal; conjunctivae pale and dry; TMs intact; tongue and mouth dry
Neck/Lymph Nodes
No JVD or HJR; no lymphadenopathy or thyromegaly
Lungs
No crackles or rhonchi
CV
Tachycardic with regular rhythm; normal S1, S2; no S3; faint S4; no MRG
Abd
Rigid with guarding, epigastric tenderness, ND; no HSM; hyperactive BS
Genit/Rect
Stool heme (+); slightly enlarged prostate
MS/Ext
Weak pulses; no peripheral edema; mild swelling of MCP joints of both hands
Neuro
A&O × 3; CNs intact; DTRs 2+; Babinski (–)
Labs
Na 132 mEq/L Ca 8.6 mg/dL
K 5.6 mEq/L Mg 2.1 mg/dL
Cl 97 mEq/L Phos 4.3 mg/dL
CO2 22 mEq/L WBC 8.6 × 103/mm3
BUN 53 mg/dL Hgb 7.6 g/dL
SCr 1.8 mg/dL Hct 22.5%
Glu 123 mg/dL Plt 96 × 103/mm3
Assessment
Admit to hospital for evaluation and management of dehydration, evaluation for acute GI bleed, and potential acute kidney injury.
Clinical Course
On admission, the patient was resuscitated aggressively with balanced crystalloids given IV and multiple transfusions (4 units of PRBCs). His home
medications were held, he was started on a continuous IV pantoprazole infusion of 8 mg/hr, and he underwent an emergent EGD. During endoscopy, a
large ulcer in the gastric antrum was found with an exposed spurting artery. Endoscopic therapy was unsuccessful, and the patient was taken to the OR
for surgical intervention. He was hypotensive in the OR (BP 70 mm Hg systolic on average) and was started on a norepinephrine infusion to maintain a
stable BP. Postoperatively, he remained on mechanical ventilation, and his urine output averaged 35 mL/hr over the first 12 postoperative hours
despite continued IV hydration and repeated transfusions in the OR. He also remained on norepinephrine for a continued low BP. On the morning of
postoperative day 1, his labs were as follows:
Na 134 mEq/L Ca 8.2 mg/dL
K 5.4 mEq/L Mg 2.2 mg/dL
Cl 111 mEq/L Phos 4.7 mg/dL
CO2 19 mEq/L WBC 14.6 × 103/mm3
BUN 49 mg/dL Hgb 10.3 g/dL
SCr 2.5 mg/dL Hct 29.8%
Glu 145 mg/dL Plt 112 × 103/mm3
Urinalysis also showed muddy brown casts, urine sodium of 72 mEq/L, and specific gravity of 1.004. The patient remained on mechanical ventilation
and norepinephrine, his urine output had not improved, and his chest radiograph showed diffuse bilateral pulmonary edema with a decrease in O2
saturation to 86%. An echocardiogram revealed hypokinesis of the anterior portion of the left ventricle and an EF of 25%. The patient was started on
dobutamine, and an internal jugular vein catheter was inserted and CVVHDF was begun.
Assessment
A 72yearold man with an acute UGI bleed, AKI, and volume overload heart failure.
QUESTIONS
Collect Information
1.a. What subjective and objective information indicates the presence of AKI postoperatively?
1.b. What additional information is needed to fully assess this patient’s AKI postoperatively?
Assess the Information
2.a. Assess the severity of AKI based on the subjective and objective information available.
2.b. Create a list of the patient’s drug therapy problems and prioritize them. Include assessment of medication appropriateness, effectiveness, safety,
and patient adherence.
Develop a Care Plan
3.a. What are the goals of pharmacotherapy for AKI in this case?
3.b. What nondrug therapies might be useful for this patient’s AKI?
3.c. What feasible pharmacotherapeutic options are available for treating AKI?
3.d. Create an individualized, patientcentered, teambased care plan to optimize medication therapy for the AKI and other drug therapy problems.
Include specific drugs, dosage forms, doses, schedules, and durations of therapy.
Implement the Care Plan
4.a. What information should be provided to the patient to enhance adherence, ensure successful therapy, and minimize adverse effects?
4.b. Describe how care should be coordinated with other healthcare providers.
FollowUp: Monitor and Evaluate
5 . Explain how to monitor and evaluate the care plan for medication appropriateness, effectiveness, safety, and patient adherence by using clinical and
laboratory data, patient feedback, and other information.
CLINICAL COURSE
On postoperative day 5, his pulmonary edema had resolved, he had been weaned off norepinephrine and dobutamine, the dialysis catheter was
removed, and he was extubated. His subsequent hospital course was uneventful, and his kidney function gradually improved.
SELFSTUDY ASSIGNMENTS
1 . Evaluate the evidence regarding the effectiveness of intravenous 0.9% sodium chloride compared to balanced crystalloids (eg, Plasmalyte, Ringer’s
lactate) in volume resuscitation for outcomes related to kidney function.
2 . Write a brief paper that discusses the utilization of intravenous sodium bicarbonate in the setting of AKI in patients who present with shock.
CLINICAL PEARL
Most laboratory markers of kidney function (eg, serum creatinine) in patients with AKI usually lag behind the true change in GFR, often by a day or
more. Therefore, adjustment of drug therapy dosing in these patients can be challenging, and often trends in urine output over the previous hours are
used to anticipate the need to make dose adjustments.
REFERENCES
Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO clinical practice guideline for acute kidney injury.
Kidney Inter Suppl. 2012;2:1–138.
Semler MW, Self WH, Wanderer JP, et al. Balanced crystalloids versus saline in critically ill adults. N Engl J Med. 2018;378(9):829–839. [PubMed:
29485925]
Prowle JR, Kirwan CJ, Bellomo R. Fluid management for the prevention and attenuation of acute kidney injury. Nat Rev Nephrol. 2014;10:37–47.
[PubMed: 24217464]
Palevsky PM. Renal replacement therapy in acute kidney injury. Adv Chronic Kidney Dis. 2013;20:76–84. [PubMed: 23265599]
Ejaz AA, Mohandas R. Are diuretics harmful in the management of acute kidney injury? Curr Opin Nephrol Hypertens. 2014;23:155–160. [PubMed:
24389731]
Kellum JA, Lameire N. Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (part 1). Crit Care. 2013;17:204. [PubMed:
23394211]
Texas Southern University Sch of Pharmacy
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1.
2.
3.
4.
5.
6.
Schwinghammer’s Pharmacotherapy Casebook: A PatientFocused Approach, 12th Edition
Chapter 54: Acute Kidney Injury: There’s Nothing Cute About It Level II
Scott Bolesta
Instructors can request access to the Casebook Instructor’s Guide on AccessPharmacy. Email Customer Success
(customersuccess@mheducation.com) for more information.
LEARNING OBJECTIVES
After completing this case study, the reader should be able to:
Assess a patient with AKI using clinical and laboratory data.
Classify AKI in a patient.
Distinguish between AKI resulting from prerenal and that from intrinsic injury.
Recommend changes to the pharmacotherapeutic regimen of a patient with AKI.
Justify appropriate therapeutic interventions for a patient with AKI.
PATIENT PRESENTATION
Chief Complaint
“I feel really weak.”
HPI
A 72yearold man presents to the ED with complaints of severe weakness that started this morning and recent stomach pain for the past week. He was
feeling well until he developed stomach pain 1 week ago that worsened with meals. Two days ago, the pain worsened to the point where he avoided
eating, and last evening he felt more tired than usual and went to bed early. He had difficulty sleeping due to the pain, and since waking this morning
he has been in too much pain and too weak to perform his normal ADLs.
PMH
HTN × 30 years
CAD × 20 years
MI × 2 with most recent 2 months ago s/p PCI with drugeluting stent placement
s/p CABG 20 years ago
HFrEF × 4 years
OA × 5 year
FH
Father died of an acute MI at age 52; mother had diabetes mellitus and died of a stroke at the age of 65.
SH
Retired and living at home with his wife. Before retirement, the patient was employed as an accountant. No alcohol, no tobacco use.
Meds
Aspirin 81 mg PO daily
Amlodipine 10 mg PO once daily
Furosemide 40 mg PO once daily
Metoprolol succinate 50 mg PO once daily
Enalapril 20 mg PO once daily
Prasugrel 10 mg PO daily
Atorvastatin 80 mg PO daily
Naproxen 500 mg PO BID
All
NKA
ROS
In addition to weakness and stomach pain, the patient complains of feeling cold but denies chills or fever. No changes in vision. Denies SOB, CP, and
cough. Complains of feeling lightheaded. Has been having frequent loose black stools over the past 3 days and abdominal pain that has become severe
in the past 2 days. Has noted a decrease in the frequency of his urination over the past 24 hours. Denies musculoskeletal pain or cramping.
Physical Examination
Gen
Pale man who appears in moderate distress and generally weak and lethargic
VS
BP 89/43 mm Hg (77/32 mm Hg on standing), P 123 bpm, RR 25, T 36.1°C; Wt 171.6 lb (78 kg), Ht 5′9″ (175 cm)
Skin
Pale and cool with poor turgor
HEENT
PERRLA; EOMI; fundi normal; conjunctivae pale and dry; TMs intact; tongue and mouth dry
Neck/Lymph Nodes
No JVD or HJR; no lymphadenopathy or thyromegaly
Lungs
No crackles or rhonchi
CV
Tachycardic with regular rhythm; normal S1, S2; no S3; faint S4; no MRG
Abd
Rigid with guarding, epigastric tenderness, ND; no HSM; hyperactive BS
Genit/Rect
Stool heme (+); slightly enlarged prostate
MS/Ext
Weak pulses; no peripheral edema; mild swelling of MCP joints of both hands
Neuro
A&O × 3; CNs intact; DTRs 2+; Babinski (–)
Labs
Na 132 mEq/L Ca 8.6 mg/dL
K 5.6 mEq/L Mg 2.1 mg/dL
Cl 97 mEq/L Phos 4.3 mg/dL
CO2 22 mEq/L WBC 8.6 × 103/mm3
BUN 53 mg/dL Hgb 7.6 g/dL
SCr 1.8 mg/dL Hct 22.5%
Glu 123 mg/dL Plt 96 × 103/mm3
Assessment
Admit to hospital for evaluation and management of dehydration, evaluation for acute GI bleed, and potential acute kidney injury.
Clinical Course
On admission, the patient was resuscitated aggressively with balanced crystalloids given IV and multiple transfusions (4 units of PRBCs). His home
medications were held, he was started on a continuous IV pantoprazole infusion of 8 mg/hr, and he underwent an emergent EGD. During endoscopy, a
large ulcer in the gastric antrum was found with an exposed spurting artery. Endoscopic therapy was unsuccessful, and the patient was taken to the OR
for surgical intervention. He was hypotensive in the OR (BP 70 mm Hg systolic on average) and was started on a norepinephrine infusion to maintain a
stable BP. Postoperatively, he remained on mechanical ventilation, and his urine output averaged 35 mL/hr over the first 12 postoperative hours
despite continued IV hydration and repeated transfusions in the OR. He also remained on norepinephrine for a continued low BP. On the morning of
postoperative day 1, his labs were as follows:
Na 134 mEq/L Ca 8.2 mg/dL
K 5.4 mEq/L Mg 2.2 mg/dL
Cl 111 mEq/L Phos 4.7 mg/dL
CO2 19 mEq/L WBC 14.6 × 103/mm3
BUN 49 mg/dL Hgb 10.3 g/dL
SCr 2.5 mg/dL Hct 29.8%
Glu 145 mg/dL Plt 112 × 103/mm3
Urinalysis also showed muddy brown casts, urine sodium of 72 mEq/L, and specific gravity of 1.004. The patient remained on mechanical ventilation
and norepinephrine, his urine output had not improved, and his chest radiograph showed diffuse bilateral pulmonary edema with a decrease in O2
saturation to 86%. An echocardiogram revealed hypokinesis of the anterior portion of the left ventricle and an EF of 25%. The patient was started on
dobutamine, and an internal jugular vein catheter was inserted and CVVHDF was begun.
Assessment
A 72yearold man with an acute UGI bleed, AKI, and volume overload heart failure.
QUESTIONS
Collect Information
1.a. What subjective and objective information indicates the presence of AKI postoperatively?
1.b. What additional information is needed to fully assess this patient’s AKI postoperatively?
Assess the Information
2.a. Assess the severity of AKI based on the subjective and objective information available.
2.b. Create a list of the patient’s drug therapy problems and prioritize them. Include assessment of medication appropriateness, effectiveness, safety,
and patient adherence.
Develop a Care Plan
3.a. What are the goals of pharmacotherapy for AKI in this case?
3.b. What nondrug therapies might be useful for this patient’s AKI?
3.c. What feasible pharmacotherapeutic options are available for treating AKI?
3.d. Create an individualized, patientcentered, teambased care plan to optimize medication therapy for the AKI and other drug therapy problems.
Include specific drugs, dosage forms, doses, schedules, and durations of therapy.
Implement the Care Plan
4.a. What information should be provided to the patient to enhance adherence, ensure successful therapy, and minimize adverse effects?
4.b. Describe how care should be coordinated with other healthcare providers.
FollowUp: Monitor and Evaluate
5 . Explain how to monitor and evaluate the care plan for medication appropriateness, effectiveness, safety, and patient adherence by using clinical and
laboratory data, patient feedback, and other information.
CLINICAL COURSE
On postoperative day 5, his pulmonary edema had resolved, he had been weaned off norepinephrine and dobutamine, the dialysis catheter was
removed, and he was extubated. His subsequent hospital course was uneventful, and his kidney function gradually improved.
SELFSTUDY ASSIGNMENTS
1 . Evaluate the evidence regarding the effectiveness of intravenous 0.9% sodium chloride compared to balanced crystalloids (eg, Plasmalyte, Ringer’s
lactate) in volume resuscitation for outcomes related to kidney function.
2 . Write a brief paper that discusses the utilization of intravenous sodium bicarbonate in the setting of AKI in patients who present with shock.
CLINICAL PEARL
Most laboratory markers of kidney function (eg, serum creatinine) in patients with AKI usually lag behind the true change in GFR, often by a day or
more. Therefore, adjustment of drug therapy dosing in these patients can be challenging, and often trends in urine output over the previous hours are
used to anticipate the need to make dose adjustments.
REFERENCES
Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO clinical practice guideline for acute kidney injury.
Kidney Inter Suppl. 2012;2:1–138.
Semler MW, Self WH, Wanderer JP, et al. Balanced crystalloids versus saline in critically ill adults. N Engl J Med. 2018;378(9):829–839. [PubMed:
29485925]
Prowle JR, Kirwan CJ, Bellomo R. Fluid management for the prevention and attenuation of acute kidney injury. Nat Rev Nephrol. 2014;10:37–47.
[PubMed: 24217464]
Palevsky PM. Renal replacement therapy in acute kidney injury. Adv Chronic Kidney Dis. 2013;20:76–84. [PubMed: 23265599]
Ejaz AA, Mohandas R. Are diuretics harmful in the management of acute kidney injury? Curr Opin Nephrol Hypertens. 2014;23:155–160. [PubMed:
24389731]
Kellum JA, Lameire N. Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (part 1). Crit Care. 2013;17:204. [PubMed:
23394211]
Texas Southern University Sch of Pharmacy
Access Provided by:
Downloaded 2024731 12:10 P Your IP is 132.174.248.24
Chapter 54: Acute Kidney Injury: There’s Nothing Cute About It Level II, Scott Bolesta
©2024 McGraw Hill. All Rights Reserved. Terms of Use • Privacy Policy • Notice • Accessibility
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