I. OBECTIVES OF CASE STUDYThe main purpose of this case presentation is to help healthcare professionals, especially nurses, to understand the causes of and the current treatments and nursing interventions for Pulmonary Congestion, Chronic Kidney Disease secondary to DM.

Specifically, this presentation aims to:

Discuss comprehensive study of the case

Define the demographics and risk profile of this disease.

Analyze the most important factors affecting the prognosis of the patients with SCC of the tongue.

Relate laboratory results with the manifestation of the disease.

Know the pathophysiology of the disease and to be able to relate signs and symptoms to the disease process

Be acquainted with the nursing interventions applicable to the patient.

Understand the importance of medical and surgical management done to the patient.

Formulate plans unique to the patient for the continuity of patient care.II. Introduction

Chronic Kidney Disease is a progressive and irreversible damage of the functioning unit of the kidneys, the nephrons. It is a progressive loss in renal function over a period of months or years. The symptoms of worsening kidney function are non-specific and might include feeling generally unwell and experiencing a reduced appetite. Often, chronic kidney disease is diagnosed as a result of screening of people known to be at risk of kidney problems, such as those with high blood pressure or diabetes and those with a blood relative with chronic kidney disease. Chronic kidney disease may also be identified when it leads to one of its recognized complication, such as cardiovascular disease, anemia or pericarditis. It is differentiated from acute kidney disease in that the reduction in kidney function must be present for over 3 months. It is identified by a blood test for creatinine. Higher levels of creatinine indicate a lower glomerular filtration rate and as a result a decreased capability of the kidneys to excrete waste products. As renal function deteriorates, nitrogen containing waste products accumulate in the blood and the uremic syndrome develops. Uremic syndrome is the cluster of clinical findings associated with the build-up of nitrogen containing in the blood, which may include fatigue diminished mental alertness, agitation, muscle twitches, cramps, anorexia, nausea, vomiting, inflammation of the membranes of the mouth, itchy skin, skin hemorrhages, gastritis, GI bleeding and diarrhea. Classification / Types Renal failure can be acute or chronic. In acute renal failure, the nephrons suddenly lose function and are unable to maintain homeostasis. On the other hand, chronic renal failure, the GFR drops suddenly and sharply. The GFR deteriorates and renal function is irreversibly altered. Chronic renal disease results from irreversible loss of large numbers of functioning nephrons. It can be categorized into five stages. The first stage is when the kidney is damaged with GFR>90 mL/min. Second stage is when GFR reaches down to 60 to 89 mL/min. In the third stage, GFR falls to 30-59 mL/min. In the fourth stage, the kidney damage is severe and the GFR is already too low reaching 15-29 mL/min. Finally in the fifth stage, the GFR already falls below 15 mL/min. In this stage, dialysis or kidney replacement is essential for the survival of the patient.III. EpidemiologyGlobally, Chronic kidney disease (CKD) is a key determinant of the poor health outcomes for major NCDs. CKD is a worldwide threat to public health, but the size ofthe problem is probably not fully appreciated. Estimates of the global burden of the diseases report that diseases of the kidney and urinary tract contribute with 830 000 deaths annually and 18 867 000 disability-adjusted life years (DALY), making them the 12th highest cause of death (1.4% of all deaths) and the 17th cause of disability (1% ofall DALY). This ranking is similar across world Bank regions, but, among developing areas, East Asia and Pacific regions have the highest annual rate of death due to diseases of the genitourinary system. National and international renal registries offer an important source of information on several aspects of CKD. In particular, they are useful in characterizing the population on renal replacement therapy (RRT) due to end-stage renal disease (ESRD), describing the prevalence and incidence of ESRD and trends in mortality and disease rates. According to this analysis, the most recent available data indicate that the prevalence of ESRD ranges from 2447 pmp in Taiwan to 10 pmp in Nigeria. However, there is paucity of renal registries globally with an international standard for registry data collection, especially in low- and middle-income countries,where, in addition, the use of RRT is scarce or non-existent, eventually making it difficultto compare ESRD results. Nationally, Manila,, Philippines In 2003, the Department of Health reported that the prevalence of chronic kidney disease (CKD) among adult =Filipinos was 2.6 percent(or 2.6 out of 100 adult Filipinos). Recent research suggests that CKD prevalence ha worsened, affecting one in 10 adult Filipinos. In 2014, the National Kidney andTransplant Institute cited kidney failure as the ninth leading cause of death among Filipinos. Consistent with worldwide statistics, the Philippine Renal Registry reports thatdiabetes is the leading cause of CKD at 44.6 percent, with hypertension as the runner-up at 4/ percent. Early detection and treatment can often keep chronic kidney from getting worsen.IV. Patient data and Health historyA. DemographicName of patient: mr. X

Age: 67 y/o

Sex: male

Civil status: married

Educational attainment:college grauduate

Occupation: retired

Religion: roman catholic

Birthday: may 27, 1947

Nationality: Filipino

B. Chief Complaints : Difficulty of BreathingInitial Diagnosis : Pulmonary Congestion

Diagnosis:Pulmonary Congestion CKD secondary to DM

Date of admission :May 25, 2015

Attending physician : DR. B Informant : Wife

C. 1. HISTORY oF Past and Present Illness

Px is 67y/o male, previously smoker and drink occassionally Hypertension 20years, ubp 11/70, hbp 130/70

type 2 DM 20 years

COPD, last attack Feb 2015, s/p intubation

CAD s/p Angioplasty 2-3 stents (feb 2014) heart center

Hemmorhagic cystitis -Feb 2015

CKD secondary to DM on MHD every MthS x 2 years

ARF secondary to CAP MR 1 week prior to admission patient complained of productive cough able to expectorate phlegm, no fever, chills noted, no medications taken.

C. 2 History of Present Illness

Day of admission px complained of undocumented fever accompannied with difficulty of breathing, sought consult to tayta doctors, CXR shows pnuemonia. Px also underwent scheduled of HD UF 5.5 Liters with minimal relief advised admission but opted to tranfer to TMC

Hypertension 20years, ubp 11/70, hbp 130/70

type 2 DM 20 years

COPD, last attack Feb 2015, s/p intubation

CAD s/p Angioplasty 2-3 stents (feb 2014) heart center

Hemmorhagic cystitis -Feb 2015

CKD secondary to DM on MHD every MthS x 2 years

ARF secondary to CAP MRD. Family History His father had hypertension, and his mother had DM.E. Review of Current Medications Seretide inhaler 125mcg 1 puff 2x a day Ventolin nebule as needed

Captopril 25mg tab 2x a day

Lanoxin tab MWF

Carvedilol 6.25mg tab once a day

Clopidogrel 75mg/tab once a day

Vestar 25mg 2x a day

F. Allergies

Allergy to SeafoodsV. Physical assessment

VI. Anatomy and physiology

The kidneys are a pair of bean-shaped organs that lie on either side of the spine in the lower middle of the back. Each kidney weighs about 5 ounces and contains approximately one million filtering units called nephrons. Each nephron is made of a glomerulus and a tubule. The glomerulus is a miniature filtering or sieving device while the tubule is a tiny tube like structure attached to the glomerulus.

The kidneys are connected to the urinary bladder by tubes called ureters. Urine is stored in the urinary bladder until the bladder is emptied by urinating. The bladder is connected to the outside of the body by another tube like structure called the urethra.

Illustration of the kidneys, urinary tract, and bladder.The main function of the kidneys is to remove waste products and excess water from the blood. The kidneys process about 200 liters of blood every day and produce about 2 liters of urine. The waste products are generated from normal metabolic processes including the breakdown of active tissues, ingested foods, and other substances. The kidneys allow consumption of a variety of foods, drugs, vitamins and supplements, additives, and excess fluids without worry that toxic by-products will build up to harmful levels. The kidney also plays a major role in regulating levels of various minerals such as calcium, sodium, and potassium in the blood.

As the first step in filtration, blood is delivered into the glomeruli by microscopic leaky blood vessels called capillaries. Here, blood is filtered of waste products and fluid while red blood cells, proteins, and large molecules are retained in the capillaries. In addition to wastes, some useful substances are also filtered out. The filtrate collects in a sac called Bowman's capsule.

The tubules are the next step in the filtration process. The tubules are lined with highly functional cells which process the filtrate, reabsorbing water and chemicals useful to the body while secreting some additional waste products into the tubule.

The kidneys also produce certain hormones that have important functions in the body, including the following:

Active form of vitamin D (calcitriol or 1,25 dihydroxy-vitamin D), which regulates absorption of calcium and phosphorus from foods, promoting formation of strong bone.

Erythropoietin (EPO), which stimulates the bone marrow to produce red blood cells.

Renin, which regulates blood volume and blood pressure. Chronic kidney disease occurs when one suffers from gradual and usually permanent loss of kidney function over time. This happens gradually, usually over months to years. Chronic kidney disease is divided into five stages of increasing severity (see Table 1 below). The term "renal" refers to the kidney, so another name for kidney failure is "renal failure." Mild kidney disease is often called renal insufficiency.

With loss of kidney function, there is an accumulation of water, waste, and toxic substances in the body that are normally excreted by the kidney. Loss of kidney function also causes other problems such as anemia, high blood pressure, acidosis (excessive acidity of body fluids), disorders of cholesterol and fatty acids, and bone disease.

Stage 5 chronic kidney disease is also referred to as kidney failure, end-stage kidney disease, or end-stage renal disease, wherein there is total or near-total loss of kidney function. There is dangerous accumulation of water, waste, and toxic substances, and most individuals in this stage of kidney disease need dialysis or transplantation to stay alive.

Unlike chronic kidney disease, acute kidney failure develops rapidly, over days or weeks.

Acute kidney failure usually develops in response to a disorder that directly affects the kidney, its blood supply, or urine flow from it.

Acute kidney failure is often reversible, with complete recovery of kidney function.

Some patients are left with residual damage and can have a progressive decline in kidney function in the future.

Others may develop irreversible kidney failure after an acute injury and remain dialysis-dependent. Table 1. Stages of Chronic Kidney Disease

StageDescriptionGFR*mL/min/1.73 m2

*GFR is glomerular filtration rate, a measure of the kidney's function.

1Slight kidney damage with normal or increased filtrationMore than 90

2Mild decrease in kidney function60 to 89

3Moderate decrease in kidney function30 to 59

4Severe decrease in kidney function15 to 29

5Kidney failureLess than 15 (or dialysis)

VII. Pathophysiology

VIII. Course in the ward

May 25, 2015

6:20pm

Admitted patient at er with gcs 15/15, bp 118/58 hr 56 rr 28 o2 sats 96% (+) crackles bilateral, pt. Given isoket drip increase to 15ml/hr, continous bp monitoring. Standby intubation if with progression of symptoms (drowziness or desaturation).

7:06

(+) drowsy, BP 105/49, O2 Sats 89%. Decrease isoket drip to 10ml/hr, Px is for stat intubation (consent secured), Given MidaZolam 5mg/iv, and Fentanyl 25mg/iv.

7:40pm

(+) drows, tachypneic , (+) crackles, BP 113/57, HR 44,

D/C isoket drip, Px is intubated w/ ET 7.5 at 22 level (+) yellowish thick secretions.

CXR -AP done

ABG 1hr post intubation

insert NGT

fastdrip 200cc IV of PNSS

Calcium Gluconate 1 amp slow iv push

7:58pm

Trop I 211.6

BP 68/38, HR 47

Fast drip another 300ml of PNSS

8:40pm

BP 86/47 HR 40

Started Levophed Drip (Levophed 16mg in 250ml PNSS to start at 10ugtts/hr

px was admitted under dr B, refer to dr p for nephro, dr v for cardio,

labs and diagnostics facilitated : cbc, na, k, ica mg ETA GS/CS, Blood CS x 2, pt, aptt, abg, CXR-AP, 12 L ecg , heplock noted at right arm

Meds : Duavent neb every 6hours, Piperracillin Taobactam 2.25g/iv every 8hours,

CBG monitoring every 4 hours

9:15

admitted at the icu

Started feeding of 1500 kcal nephro based DM continous feeding at 62.5ml/hr + 30ml water flushing every 8hours

Head of bed 30-45

decreased FIO2 to 60%

2d echo defer (relative)

Hold Carvedilol, Lanoxin and Captopril for now

start Fluimucil 600mg/tab 1 ta in glass of water 2x aday/ngt

apply 2 point restraints

if with agitation pls start precedex dip for sedation

include serum cortisol, uric acid to bloodworks

rpt cbc and serum k tom post bt

CBG 3x a day

hold insulin for now

Pt is for HD on thurs (may 28)

9:26pm

ph 7.423, pc02 37.8, P02 291.1, Bicarb 24.9, 02 Sats 99..9% - decreased FIO2 to 40%

May 26, 2015

1:15am

Px cough out the ET tube, Monitored patient, On standy by re-entubation.

Px re-intubated, midazolam 1mg/iv given for pre medications

1:55am

requested for CXR to confirm ET is on top of location

Started midazolam drip 30mg in 30ml of D5W to start at 1mg/hr ( hold if with hypotension)

7:00am

for sled on thursday

give piperacillin tazobactam of 0.75mh/iv after HD

Started Esomeprazole 40mg/iv now then once daily

nebulize with salbutamol every 8hours

start enoxaparin 0.2ml once daily

8:00am

still with Low blood pressure and bradycardia

titrated levophed

given albumin 20% 1vial + 200ml PLR bolus, but still no improvement

recommend dopamine instead of norephineprine

continue duavent neb every 6hours hold salbutamol

11:15

Started dopamine drip 20ml in 250ml PNSS in 2mg/kg/min and titrate to target MAP of >70.

Re Scheduled pt. dialysis tom and friday 8 hours,

transfuse 2units PRBC during dialysis, properly typed and crossmatched

4:00pm

maintained MV settings

Give Vancomycin 1g in 100ml PNSS to sun for 2 hours

7:00pm

Started Lactulose 30ml once a day at bbedtime

shift esomeprazole to Pantoprazole 40mg/iv

increase midaolam to 1.5ml/hr

apply 2 point restrants

May 27 2015

Changed MV setting to FIO@ 35, PS 12

for cxr ap sitting after HD

decreased duavent neb to every 8hours

Start Vancomycin 500mg every @ days diluted in 100 ml PNSS to run for 1 hour,,

on dialysis days give vancomycin 2grams diluted in 200ml PNSS at 15mg/min over the last 2 hours of dialysis

facilitate BT

continue piperacillin tazobactam

Budesonide 500mcg 1 nebule every 12hours

titrate dopamine drip to Map >65

for cbc tom include na, k , mg

Shifted vancomycin to oxacillin 2grams every 6hours

May 28, 2015

For HD tomorrow (friday), 8hours duration

for 2d echo with DS done

Done ABG

Maintianed MV settings, and o2 sats >94%, for passive leg raise

Start Lactulose 30 ml once daily- hold if with BM 2x a day

shifted pantopraole to lansopraole 30mg/tab once a day per ngt

revise feeding to 1500kcal nephro baased DM 2:1dilution with 20ml flushing every 4 hours

increased duavent neb to every 6hours

continue suctions thick secretions

maintained present vent setting for now

for abg, lactate tom morning and include cortisol, and phospuros

May 29, 2015

please apply 2 point restraints

for repeat CXR post HD

for rpeat cbc pre HD

please reserve 1u PRBC properly typed and crossmatched for possible transfusion during HD

Start Hydrocortisone 200mg/iv in 200ml PNSS for 24hours

Facilitate HD

decreased PS to 10

decreased duavent neb to every 8hours and as needed

continue oxacillin and piperacillin taobactam,

IX. Drug study

X. Diagnostic exams and results

XI. Nursing care plan

PROBLEMGOAL OF CAREINTERVENTIONEVALUATION

INEFFECTIVE AIRWAY CLEARANCE RELATED TO (+) YELLOW THICK SECRETION Objective:

-yellowish thick secretion

-crackles at bilateral lower segment

-with Endotracheal tube with closed suctionAfter 8 hours, the patient will have no signs of respiratory distress and desaturation, and maintain airway patency.Assess respiratory rate and secretions

Auscultate bilateral lower segment of the lungs

Elevate head of bed

Turn patient side to side every 2 hours

Suction secretion as needed

Administer mucolytics as prescribed

Perform nebulization as ordered

Perform chestphysiotherapy (back tapping)

After 8 hours, the patient noted no signs of respiratory distress and desaturation, and airway patency maintained.

PROBLEMGOAL OF CAREINTERVENTIONEVALUATION

FLUID VOLUME EXCESS RELATED TO PULMONARY CONGESTION

Objective:

-crackles at bilateral lower segment

- (+) agitation

(+) drows, tachypneic ,

Shortness of breath

BP-111/58

HR 56

RR 28

o2 sats 96%After 8 hours, patient will have no signs of respiratory distress and desaturation, and maintain airway patency.Assess respiratory rate and secretions

Auscultate bilateral lower segment of the lungs

Elevate head of bed

Turn patient side to side every 2 hours

Monitor input and output accuratelyAfter 8 hours, the patient noted no signs of respiratory distress and desaturation, and airway patency maintained.

XII. Discharge planning