Bloody Report

Case Management

Presented By: Trina Marie Montemar- Majam M.D.

General Data • • • • •

E. M 23 yr old male non hypertensive, non diabetic admitted in our institution on Sept 22, 2009 • chief complaint: loose bowel movement.

History of present illness • 3 days PTA • after drinking tap water in an amusement park, noted loose bowel movement, described as watery, yellowish in color, foul smelling, non mucoid, non bloody x 1 episode. • No other s/sx noted such as vomiting or fever. • No medications taken.

History of Present Illness • 2 days PTA • loose bowel movement was noted to be persistent described as non mucoid, non bloody, foul smelling about 10 episodes • associated with 5 episodes of non projectile vomiting of previously ingested food, crampy abdominal pain localized on epigastric area. • No medications taken, no consult was done.

History of Present Illness • 1 day PTA, still persistent loose bowel movement, >10 episodes prompted consult w/ private doctor • . Fecalysis was done and revealed normal results, however he was prescribed w/ Metronidazole 500mg/tablet, 1 tablet TID, Domperidone 10 mg/tab, 1 tablet TID. • At home symptoms persisted. • Patient replaced losses with increase intake of oral fluids.

History of Present Illness • 4 hours PTA • still with LBM same character as above for > 10 episodes associated with 5 episodes of vomiting of previously ingested food prompted consult at our institution and was admitted.

Past Medical History • Unremarkable

Family Medical History • (+) Hypertension – father/mother • (+) DM- paternal side

Personal & Social History • Works as a banker • Non cigarette smoker • Non alcohol beverage drinker

Review of systems • • • • •

(-) wt loss (-) difficulty of breathing (-) chest pain (-) fever (-) dysuria

PHYSICAL EXAMINATION • General Survey: awake, conscious, coherent, not in cardiorespiratory distress • Vital Signs :BP= 110/80 mmHg, HR 73 bpm, RR=22, T=36.3 • Skin:no skin lesions, good turgor and mobility • HEENT: pink palpebral conjunctiva, anicteric sclera, dry lips, dry oral mucosa, no CLAD

PHYSICAL EXAMINATION • Chest & Lungs: SLE, no retractions, clear and equal breath sounds • Heart: Adynamic precordium, normal rate, regular rhytym, no murmur • Abdomen: flabby,hyperactive bowel sounds, tympanitic, non tender, soft, • Extremities:full, equal pulses, no edema

COURSE IN THE ER • Vital Signs: BP= 100/ 70 mmHg PR=82 bpm RR=22 T= 36.9 • DIET: NPO temporarily • IVF: PNSS 1L x 8 • Laboratory Procedures: CBG, CBC, Serum Na, K, Bun & Crea,Fecalysis, Urinalysis, FBS & Lipid profile • Medications: Metronidazole 500 mg IV q 8 Metoclopromide 10 mg IV q8 prn for vomiting Omeprazole 40 mg IV OD Hydrite tablet, 2 tablets in 200 ml water as tolerated, volume/volume replacement

COURSE IN THE ER • While at the ER awaiting transfer, pt has sudden onset of difficulty of breathing. • On PE, pt was noted to be tachycardic and tachypneic. • Pt was rendered o2 inhalation at 2-3 lpm. • Laboratory procedures such as ABG, CXR, 12 L ECG, CKMB, Trop I were done. • Pt for ICU admission.

RENAL FAILURE • Acute Renal Failure • Chronic Renal Failure

INCIDENCE • The mortality rate estimates vary from 25-90%. • The in-hospital mortality rate is 4050%. • in intensive care settings, the rate is 70-80%.

Mortality • The mortality rate estimates vary from 25-90%. • The in-hospital mortality rate is 4050%. • in intensive care settings, the rate is 70-80%.

DEFINITION OF TERMS • BUN (blood urea nitrogen) is synthesized mainly in the liver – the end product of protein catabolism.

• Increased BUN: dehydration, GI bleeding, cell lysis, steroid usage, increased dietary protein, decreased renal perfusion (CHF, renal artery stenosis). • BUN to creatinine ratio is 10:1. – Dehydration can increase to 20:1 or higher.

• Decreased BUN: liver disease and in the syndrome of inappropriate antidiuretic hormone secretion (SIADH).

DEFINITION OF TERMS • BUN is an indirect and rough measurement of renal function and glomerular filtration rate. • It is also a measurement of liver function. • Urea is formed in the liver as the end product of protein metabolism and digestion. • Normal findings; Adult: 10-20 mg/dl; Child 5-18 mg/dl

Definition of Terms • Creatinine – is a product of muscle metabolism produced and cleared by the renal excretion. – is used to diagnose impaired renal function. This test measures the amount of creatinine in the blood.

DEFINITION OF TERMS • Glomerular Filtration Rate (GFR) – provides a useful index of overall renal function, but some pts. have a normal or increased GFR. – It measures the amount of plasma ultrafiltered across the glomerular capillaries and correlates with the ability of the kidneys to filter fluids and various substrates.

DEFINITION OF TERMS In clinical practice, the clearance rate of endogenous creatinine, the creatinine clearance, is the usual means of estimating GFR.

Uremia Uremia is the clinical syndrome associated with the retention of the end products of nitrogen metabolism that occurs with severe reduction in renal function.

In uremia, the presence of symptoms is unusual before the blood urea nitrogen (BUN) level reaches 60mg/dl or when the serum creatinine level is 8mg/dl. The BUN value typically correlates most strongly with uremic symptoms and may indicate acute or chronic renal failure as well as serum and urine creatinine levels.

PATHOPHYSIOLOGY • AKI may occur in 3 clinical patterns, including the following: (1) as an adaptive response to severe volume depletion and hypotension, with structurally intact nephrons; (2) in response to cytotoxic, ischemic, or inflammatory insults to the kidney, with structural and functional damage; and (3) with obstruction to the passage of urine

PATHOPHYSIOLOGY Adaptive response to severe volume depletion and hypotension with structurally intact nephrons

Prerenal

Pathophysiology In response to cytotoxic, ischemic and inflammatory response to insults in the kidney with structural and functional damage

intrinsic

Pathophysiology

Obstruction to passage of urine

Post renal

ACUTE RENAL FAILURE

PRERENAL

INTRINSIC

POST RENAL

PRE RENAL • Causes renal hypoperfusion resulting in decrease in function • Without frank parenchymal damage • 55% • Most common • Generally reversible

Major Causes of Prerenal ARF • Hypovolemia • Altered renal hemodynamics

HYPOVOLEMIA • • • • •

Increased ECF loses GI fluid loss Renal Fluid Loss Extravascular sequestration Decreased intake

Altered Renal Hemodynamics • • • •

Low cardiac output state Systemic Vasodilatation Renal Vasoconstriction Impairment of renal autoregulatory responses • Hepatorenal Syndrome

INTRINSIC • Directly involve the renal parenchyma • 40%

Major Causes of Intrinsic ARF • Renovasular obstruction • Disease of the glomeruli or vasculature • Acute tubular necrosis • Interstitial nephritis • Intratubular obstruction

POST RENAL • Associated with urinary tract obstruction • 5%

Major Causes of Post Renal ARF • Ureteric • Bladder neck • Urethra

SIGNS AND SYMPTOMS • Pre renal – Hx of poor fluid intake, tx with NSAIDS or ACE Inhibitors, heart failure – s/sx of volume depletion

SIGNS AND SYMPTOMS • Intrinsic ARF – Diseases of the renal vessels – ATN – Disease of the tubulointerstiutium

SIGNS AND SYMPTOMS • Post renal ARF – History of renal stones or prostatic disease

DIAGNOSIS • Consensus criteria (RIFLE) for the diagnosis of ARF are: • Risk: serum creatinine increased 1.5 times OR urine production of <0.5 ml/kg body weight for 6 hours • Injury: creatinine 2.0 times OR urine production <0.5 ml/kg for 12 h • Failure: creatinine 3.0 times OR creatinine >355 μmol/l (with a rise of >44) or urine output below 0.3 ml/kg for 24 h • Loss: persistent ARF or complete loss of kidney function for more than four weeks

Diagnostic Procedures • complete blood cell count • urine analysis with microscopy, and urine electrolytes. • Blood urea nitrogen and serum creatinine

Diagnostic Procedures • Ultrasound – Renal ultrasonography is useful for evaluating existing renal disease and obstruction of the urinary collecting system. The degree of hydronephrosis does not necessarily correlate with the degree of obstruction. Mild hydronephrosis may be observed with complete obstruction if found early. – Obtaining images of the kidneys can be technically difficult in patients who are obese or in those with abdominal distension due to ascites, gas, or retroperitoneal fluid collection. – Ultrasound scans or other imaging studies showing small kidneys suggest chronic renal failure.

Diagnostic Procedure • Doppler scans – Doppler scans are useful for detecting the presence and nature of renal blood flow. – Because renal blood flow is reduced in prerenal or intrarenal AKI, test findings are of little use in the diagnosis of AKI. – Doppler scans can be quite useful in the diagnosis of thromboembolic or renovascular disease. – Increased resistive indices can be observed in patients with hepatorenal syndrome.

Diagnostic Procedures • Nuclear scans

– Radionuclide imaging with a technetium Tc 99m diethylenetriamine pentaacetic acid (DTPA), 99m TcDTPA iodine I 131–hippuran scan can be used to assess renal blood flow and tubular functions. – Because of a marked delay in tubular excretion of radionuclide in both prerenal disease and intrarenal disease, the value of these scans is limited. – Aortorenal angiography can be helpful in establishing the diagnosis of renal vascular diseases, including renal artery stenosis, renal atheroembolic disease, atherosclerosis with aortorenal occlusion, and in certain cases of necrotizing vasculitis (eg, polyarteritis nodosa).

Diagnostic Procedures • Imaging: In addition to renal ultrasonography, other imaging tests are occasionally of use. In evaluating for ureteral obstruction, a noncontrast CT scan is preferred over antegrade and retrograde urography. In addition to its ability to delineate soft-tissue structures and Ca-containing calculi, CT can detect nonradiopaque calculi.

Diagnostic Procedures • Contrast agents should be avoided if possible. However, renal arteriography or venography may sometimes be indicated if vascular causes are suggested clinically. Magnetic resonance angiography was increasingly being used for diagnosing renal artery stenosis as well as thrombosis of both arteries and veins because MRI used gadolinium, which was thought to be safer than the iodinated contrast agents used in angiography and contrast-enhanced CT.

DIAGNOSTIC PROCEDURES • Kidney size, as determined with imaging tests, is helpful to know, because a normal or enlarged kidney favors reversibility, whereas a small kidney suggests chronic renal insufficiency

Management • Goal – recognizing the presence of AKI and promptly initiating therapy aimed at minimizing the damage to the remaining functional renal mass are important considerations. This may also aid in reversing the renal damage that has already occurred. Reversing renal damage can be accomplished only by identifying the underlying cause and directing the appropriate therapy.

Management • Maintenance of volume homeostasis and correction of biochemical abnormalities remain the primary goals of treatment. • Furosemide

Management • Correcting hematologic abnormalities (eg, anemia, platelet dysfunction) warrants appropriate measures, including transfusions and administration of desmopressin or estrogens

Management • Dietary modulation is an important facet of the treatment of AKI. Diet and fluid restriction become crucial in the management of oliguric renal failure, wherein the kidneys do not adequately excrete either toxins or fluids.

Management • Vasodilators • Calium Channel Blockers

Management • Dialysis • Indications for dialysis in patients with AKI are as follows: – Volume expansion that cannot be managed with diuretics – Hyperkalemia refractory to medical therapy – Correction of severe acid-base disturbances that are refractory to medical therapy – Severe azotemia (BUN >80-100) – Uremia

PROGNOSIS • Although many causes are reversible if diagnosed and treated early, the overall survival rate remains about 50% because many patients with ARF have significant underlying disorders (eg, sepsis, respiratory failure). • Death is usually the result of these disorders rather than the renal failure itself.

Prognosis • Most survivors have adequate kidney function. • About 10% require dialysis or transplant—half right away and the others as renal function slowly deteriorates.

Lab results • • • • •

Bun 10.5 Crea 259 Na 139 K 3.5 CBC Hct- .60 Hgb 193 wbc 17.4 seg .82, lymph .12, platelet adequate

Lab Results • ABG: pH 7.062, PC02 24, PO2 108.1, 02Sat 96.1, HCO3 6.4 • CKMB: 20 • Troponin I :<0.01 • CXR: Normal Chest • 12 L ECG: