FIRST CLINICAL CASE STUDY 1

Acute Kidney Injury (AKI)

Joida Mae Esper I. Canono 22030085

ENP 110 Nursing Practicum II

Clinical Instructor Robbi Martson

February 6, 2023
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Acute Kidney Injury

History of Present Illness

Mr. W. J. G. is an 82-year-old, male patient who was admitted to the hospital with

clinical manifestations of altered level of consciousness and unwitnessed fall.

Patient last seen at baseline 2 days ago, according to report. His daughter discovered him

on the ground this afternoon with a changed state of consciousness, mumbled speech, and a

refusal to respond to questions. There are no evident extremities deformities or evidence of head

damage. No more information about the past was currently available. She later informed the

medical staff that the patient had a TURP for an enlarged prostate and had been sent home.

Patient due to arrive and confirm with patient I did not. No seizures were observed.

Past Medical History

1. Atrial Fibrillation

2. Hypertension

3. Non-insulin-dependent diabetes

Social History

 His wife passed away last year, leaving him to live alone, and he has been gradually

struggling to carry out duties of daily living.

Medical Diagnosis:

Urosepsis, Acute Kidney Injury

Pathophysiology

Severe and dysregulated inflammation in response to infection, known as sepsis, is

defined by end-organ dysfunction that occurs away from the main infection site. Acute kidney
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injury (AKI) that develops during sepsis affects numerous organ functions significantly, raises

the risk of mortality, and increases patient morbidity.

In this case, patient presented with hypoactive delirium which is a secondary to sepsis.

This is a case, blood supply to crucial organs, including brain, heart, and kidneys, is hampered as

sepsis worsens. As evidenced by his laboratory findings: White count 11.7, hemoglobin 113 and

platelets 230. Predominantly neutrophils. MCV 78 and RDW of 14.9. Reveals a normal pH of

7.38. Sodium 126 with a potassium of 5.1. Creatinine 209 and troponin elevated at 181. Calcium

normal at 2.31. Urinalysis: Leukocyte esterase positive, bacteria positive, nitrate negative. ECG:

Sinus tachycardia with no ST changes. Q waves are seen in inferior leads.

S-AKI is attributed to decreased global renal blood flow and acute tubular necrosis, or

secondary tubular epithelial cell death. The host reaction drives and characterizes sepsis and its

severity, while the bacterial infection is responsible for the disease's initial onset. The patient in

this instance already has underlying conditions like hypertension, BPH, and DM. When the

proteins of the microbial pathogen contact with those of the host's cell membrane, the

immunological response of the host is set off. The development of edema, enhanced neutrophil

production that produces bactericidal chemicals, and cell necrosis are all possible outcomes of a

severe pro-inflammatory response. After this initial stage, the body experiences an anti-

inflammatory reaction that causes immunosuppression, which causes neutrophils to malfunction

and further harm neighboring cells, that is also reflected to patient’s laboratory findings.
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Care Plan

Code Status: DNR

Admitting Diagnosis: UROSEPSIS / AKI

Allergies: CODEINE

Surgical intervention: TURP (Transurethral resection of the prostate)

Coexisting Illness(es): Hypertension, BPH with recent TURP, Non-insulin-dependent diabetes

Diet: REGULAR

Oxygen: ROOM AIR

Isolation: DROPLET/CONTACT

Dressing: A. Coccyx and buttocks - Hygeol 1:20 solution to eschar x 15 mins

- apply inadine

Activity: Mobility level C

Lift/Transfer: Dependent

Level of Risk for Falls: High

Tubes: IFC

Pressure Area condition: Has a necrotic tan base with a small patch of black necrosis, a solid

pressure injury to mid-spine, and no open or draining areas. He has also a pressure injury to the

buttocks that is irregularly shaped, has a yellow adherent slough at the base, limited drainage,

and pink, painful skin around the wound.