Azotemia and urinary abnormalities

Assessment of GFR (Glomerular Filtration Rate)

• Primary metric for kidney function

• Serum creatinine– used as surrogate to estimate GFR; most widely used for drug dosing and grading of chronic

kidney disease

• Low GFR leads to azotemia (retention of Creatinine, BUN, and nitrogenous wastes increase serum BUN and

Creatinine)

• Uremia (azotemia with signs and symptoms) will develop at significantly different levels of creatinine

• Signs and symptoms: n/v, change in sensorium

• Related directly to urine creatinine excretion and inversely to serum creatinine (Creatinine Clearance)

Estimation of Glomerular Filtration Rate

Cockcroft-Gault:

Creatinine clearance (mL/min)

= (140-age) x lean body weight (kg)

Plasma creatinine (mg/dL) x 72

** Multiplied 0.85 for women

MDRD: (modification of diet in renal disease)

GFR = 186 x Serum Creatinine -1.154

x Age-0-203

x [1.210 if Black] x [0.742 if Female]

Other ways of determining GFR:

Direct GFR

o Inulin clearance

o Iothalamate- available in La Salle; used in renal GFR scan

EDTA

Cystatin C- member of cysteine protease inhibitors and is produced at a relatively constant rate from all nucleated

cells.; more sensitive marker of early GFR decline than plasma creatinine

Chronic renal failure

Define as increase creatinine for more than 3 months

Small kidneys + normal urinalysis + increase creatinine

3 major causes:

o Diabetic nephropathy

o Amyloidosis

o HIV nephropathy

Acute Renal Failure

• Categories

o Pre-renal

Before renal

Any condition that can cause hypoperfusion of kidney leading to azotemia

Accounts for 40-80% of ARF and readily reversible if treated early

Causes:

• Decreased circulating blood volume (GI hemorrhage, burns, diarrhea, diuretics)

• volume sequestration(pancreatitis, peritonitis, rhabdomyolysis)

• decreased effective arterial volume (hypotension, cardiogenic shock, sepsis)

• Peripheral vasodilation ( sepsis, drugs)

• Profound renal vasoconstriction (severe heart failure, hepatorenal syndrome, NSAIDs[prostaglandin

production blockade], ACE-Is, and ARBs[decreased efferent arteriolar tone decreased glomerular

capillary perfusion])

• Renal stenosis

Subject: Medicine Topic: Cardinal Manifestation of Renal Disease

Lecturer: Dr. M. Bernardo

Date of Lecture: 01/28/2012

Transcriptionist: kekie and dj anne

Pages: 14

SY 2

011-2

012

o Intrinsic

Causes

• Acute Tubular Necrosis

o Ischemic

Common in patients that have undergone major surgery, trauma, severe hypovolemia,

overwhelming sepsis, or extensive burns

o Nephrotoxic

Complicates the administration of many common medications, usually by inducing a combination

of intrarenal vasoconstriction, direct tubule toxicity, and/or tubule obstruction

Remember that kidneys have a rich blood supply (25% of CO) and one of its function is to

concentrate, and metabolize toxin, henceforth making it susceptible to toxins.

• Interstitial nephritis

Drug-induced interstitial nephritis (antibiotics, NSAIDs, diuretics, Chinese medication chronic use)

Severe infections (bacterial and viral)

Systemic infections (SLE)

Infiltrative disorders (sarcoid, lymphoma, leukemia)

Allergic interstitial nephritis (eosinophils in urine)

Urinalysis: mild to moderate proteinuria, hematuria, and pyuria; occasionally WBC casts

• Renovascular obstruction

• Glomerulonephritis or vasculitis

o Post-renal- obstructive

Reversible, <5% of ARF

Ureteral and renal pelvic dilatation on ultrasound

Causes

• Urethra or bladder outlet obstruction

• Bilateral or unilateral ureteral obstruction

Table on the left compares the laboratory findings in acute renal failure, prerenal vs oliguric acute renal failure (intrinsic). In prerenal azotemia, urine sodium is less than 20 and the fractional excretion of Na is <1%, which indicates that it is still able to conserve sodium and its reabsorption is still intact, respectively. Intrinsic azotemia on the other hand, has sodium wasting leading to increased UNa [>40] and FENa [>2%].

Picture on the left showing hydronephrosis. Notice how the ureter, renal pelvic are dilated on the rt side.

In patient with azotemia, presence of hydronephrosis (dilation of renal tract.) is determined by renal ultrasound. If present,

this is likely to be caused by post-renal azotemia- obstruction; and patient is managed by urologic evaluation and relieving

such obstruction. If hydronephrosis is absent, urinalysis is done along with the determination of the size of renal parenchyma

to differentiate chronic renal failure from acute renal failure. Small kidneys, thin cortex, bland sediment (unremarkable

microscopic determination), isosthenuria and <3.5g/24 hours protein is indicative of chronic renal failure. A normal size

kidney and intact parenchyma on the other hand is indicative of acute renal failure (as discussed above can be divided into

pre-renal, intrinsic, and post-renal). Normal kidney with abnormal urinalysis may indicate acute tubular necrosis,

glomerulonephritis, renal vessel occlusion, interstitial nephritis, and pyelonephritis depending on the abnormal sediments

seen. Urine electrolytes and osmolality must be tested if kidney and urinalysis are both normal. If urine osmolality is >500

mosmol and fractional sodium excretion is <1%, its indicative of prerenal azotemia. FeNa>1% and U osmo <350mosmol with

normal or abnormal urinalysis (muddy brown cast) is indicative of acute tubular necrosis.

ABNORMAL URINALYSIS: Note that if >100,000 of bacteria is present in the urine, it may be indicative of pyelonephritis. WBC

cast is indicative of Interstitial nephritis. Presence of RBC can indicate Artery or venous occlusion and can be confirmed by

angiogram. RBC cast with proteinuria may indicate Glomerulonephritis and can be confirmed by renal biopsy.

Proteinuria

• Dipstick determination

• Normal <150 mg/day of total protein and <30 mg/day of albumin

• Positive dipstick on urinalysis detect predominantly albumin; cannot detect urine albumin levels < 300 mg/d

indication: can only detect macroalbuminuria

• Microalbuminuria:

o 30-300 mg/d or 30-300 mg/g

o Please see the diseases to be considered on the algorithm below

• Macroalbuminuria with RBC casts or RBCs on urinalysis:

o 300-3500 mg/day or 300-3500 mg/g

o Please see the diseases to be considered on the algorithm below

• Macroalbuminuria (Heavy proteinuria):

o > 3500 mg/d or 3500 mg/g Nephrotic syndrome (recall:s/s heavy proteinuria + dyslipidemia + edema)

o Please see the diseases to be considered on the algorithm below

• Urine protein electrophoresis can classify pattern of proteinuria (as glomerular, tubular, abnormal proteins)

o Glomerular proteinuria (can be selective or nonselective) – due to abnormal glomerular permeability

o Tubular proteins (TH, B2-macroglobulin) are produced by the renal tubule and shed into the urine caused

by tubular injury, HPN, and CRF.

o Abnormal circulating proteins (light chains and Bence Jones protein) are readily filtered because of their

small size can be cause by blood cell dyscrasias such as Multiple Myeloma

Hematuria

Normal RBC excretion – 2 million RBC/day

Hematuria – 2-5 RBC/hpf

Common causes:

o Stones

o Neoplasms

o Tuberculosis

o Trauma

o Prostatitis

Gross hematuria w/ blood clots - post renal source

Single urinalysis with hematuria is common.

o Menstruation

Always r/o in women

o Viral illness

o Allergy

o Exercise

o Mild trauma

Persistent hematuria

o >3RBC/hpf on 3 urinalysis or single urinalysis

with >100 RBCs, or gross hematuria

o Considerations:

Chronic anticoagulation

Urogenital neoplasms

Infection

Hypercalciuria, hyperuricosuria

Hematuria without proteinuria and dysmorphic RBCs or RBC casts but with pyuria and WBC casts is indicative of UTI and confirmed by urine culture. Hematuria with proteinuria and dysmorphic RBCs and RBC casts indicates glomerulonephritis and can be further evaluated with serologi, hematologic examinations and renal biopsy. Hematuria + (-) proteinuria + (-) pyuria:

(+) IVP +/- renal ultrasound stones, renal cysts

(+) cystoscopy bladder neoplasm needing biopsy and evaluation

(+) renal CT scan renal neoplasm, renal cell CA All negative, follow-up periodic urinalysis PYURIA AND CASTS

Isolated pyuria is unusual since inflammatory

reactions in the kidney are also associated with

hematuria.

Waxy Casts - degenerated cellular cast

Broad Casts - dilated tubule of enlarged

nephrons

ABNORMALITIES OF URINE VOLUME

Oliguria and Anuria

Oliguria - urine output of <500 ml/24hr

Anuria –urine output of < 50 ml/24 hr

o Causes

Total urinary tract obstruction (note

that obstruction to just one kidney will

not cause anuria since one kidney is

enough to maintain kidney function)

Total renal artery or vein occlusion

Shock

Cortical necrosis, ATN and RPGN

Nonoliguria: >500 ml/day in patients with acute

or chronic azotemia

Polyuria

Remember polyuria is INCREASED in VOLUME

and not increased in frequency

Should be differentiated from urinary frequency

– small volumes

24 hour urine collection, urine output is >3L/day

Mechanisms:

o Excretion of nonabsorbable solutes

o Excretion of water (defect in ADH

production or renal responsiveness)

Urine osmolality

o solute diuresis (excretion of nonabsorbable

solutes), high urine osmolality

o water diuresis (excretion of water), low

urine osmolality

Check urine osmolality

If patient is excreting a urine high in osmolality, it means that the polyuria is caused by solute diuresis. There are

solutes in the renal tubules that causes the water to stay in the renal tubules and move out of the body as urine.

If the patient is excreting a dilute urine, then the polyuria is from water diuresis.

Water deprivation test will distinguish between primary polydipsia versus diabetes insipidus.

If you decrease the water intake of a patient and the results is correction of polyuria, then the cause of polyuria is a

primary polydipsia. Drugs and hypothalamic disease all cause increase in water intake by changes in the brain. Primary

polydipsia may also be caused by psychogenic processes.

Diabetes insipidus is divided into 2 types: central and nephrogenic.

To differentiate between the 2 causes of DI, ADH level is needed.

Low ADH level means px is experiencing Central DI, and the polyuria will correct with administration of exogenous

vasopressin.

Normal to high ADH points to a nephrogenic DI. Even with exogenous vasopressin, polyuria from vasopressin will not

resolve since nephrogenic DI is caused by insensitivity of the renal tubules to vasopressin.

FLUID AND ELECTROLYTE DISTURBANCE

Sodium and Water

Composition of Body Fluids

Water - most abundant constituent of the body.

50% of body weight in women, 60% in men

Osmolality - solute or particle concentration of a

fluid

Major ECF particles are Na+ and its accompanying

anions Cl- and HCO3

-

Major ICF osmoles: K+ and organic phophate esters

(ATP, creatine phosphate, and phospholipids) Ineffective osmoles - do not contribute to water shift eg. Urea, glucose

Water Balance

Normal plasma osmolality is 275-290 mosmol/kg

Water intake = water excretion

Disorders in water homeostasis:

o Hyponatremia

o Hypernatremia

Water Intake

THIRST – primary stimulus for water ingestion

Ineffective osmoles do not play a role in stimulating

thirst.

Average osmotic threshold for thirst is approx. 295

mosmol/kg

Water Excretion

Arginine vasopressin (AVP) – principal determinant

of renal water excretion

HYPERTONICITY - major stimulus for AVP secretion

Major ECF solutes are Na salts, effective osmolality is

primarily determined by plasma Na concentration.

Inc Na inc AVP secretion

Nonosmotic factors that affect AVP secretion:

◦ Effective circulating (arterial) volume

◦ Nausea

◦ Pain

◦ Stress

◦ Hypoglycemia

◦ PregnancyDrugs (e.g. morphine)

Sodium Balance

Sodium is actively pumped out of cells by Na-K-

ATPase pump.

Hence, 85-90% of all Na is extracellular.

Na loss = Na gain

Na excess edematous state

Na deficit hypovolemic state

Hypovolemia

Clinical Features

Nonspecific and secondary to electrolyte imbalances

and tissue hypoperfusion

o Fatigue, weakness, muscle cramps, thirst,

postural dizziness

More severe degrees of hypovolemia End-organ

ischemia

o manifest as oliguria, cyanosis, abdominal and

chest pain, confusion or obtundation

Treatment

Mild – oral route

More severe – requires IV therapy with isotonic or

normal saline

Hypernatremia – greater deficit of water than Na

o Tx: hypotonic solution such as half-normal saline

or D5W

Pxs w/ sig. hemorrhage, anemia or intravascular

volume depletion: BT or colloid-containing solutions

(albumin, dextran)

HYPONATREMIA

• Plasma Na conc of < 135 mmol/L

• Not a disease but a manifestation

Clinical Features

Related to osmotic water shift leading to increased

ICF volume

Sxs primarily neurologic

o Brain cell swelling or cerebral edema

Severity is dependent on rapidity of onset and

absolute decrease in plasma Na conc.

Asx, or complain of nausea and malaise

As plasma Na conc falls, sxs progress

o Headache, lethargy, confusion, and obtundation

Plasma Na conc falls acutely below 120 mmol/L or

decreases rapidly

o Stupor, seizures, and coma

Treatment of Hyponatremia

Mild asymptomatic hyponatremia requires no

treatment.

Asx hyponat + volume contraction isotonic saline

Hyponat due to edematous states restriction of

Na and water intake

Rate of correction of hyponat depends on absence

or presence of neurologic dysfunction.

No neurologic dysfunction

Plasma Na conc should be raised by no more than

0.5-1.0 mmol/L per hr and by < 10-12 mmol/L over

the first 24h

Severe symptomatic hyponat

Treated with hypertonic saline

Plasma Na conc should be raised by 1-2 mmol/L per

hour for the 1st

3-4 hrs until seizures subside.

Plasma Na conc should be raised no more than 12

mmol/L during the 1st

24 hours

Osmotic Demyelination Syndrome (ODS)

Caused by correcting hyponatremia rapidly

Neurologic disorder characterized by flaccid

paralysis, dysarthria and dysphagia

No specific treatment

Assoc. w/ increase morbidity and mortality

HYPERNATREMIA

Plasma Na conc of > 145 mmol/L

Majority due to loss of water

Clinical Features

Hypertonicity water shifts out of cells leading to

contracted ICF volume

Decreased brain cell volume is assoc with increased

risk of subarachnoid or intracerebral hemorrhage.

Treatment

Goal:

1. Stop ongoing water loss (treat underlying cause)

2. Correct water deficit

Water deficit = Plasma Na conc – 140 x TBW

140

Treatment

GIT – safest route of water administration

IV – using D5W or hypotonic saline

CDI – desmopressin

Sxic polyuria due to NDI – low-Na diet and thiazide

diuretics

POTASSIUM

HYPOKALEMIA

Plasma K conc of < 3.5 mmol/L

Etiology

Redistribution into cells – metabolic alkalosis and

insulin

Nonrenal loss of K

o Excessive sweating, diarrhea

o Renal loss of K

o Primary hyperaldosteronism, Liddle’s syndrome,

Bartter’s syndrome, RTA

Clinical Features

Fatigue, myalgia and muscular weakness of the

lower extremities are common complaints.

o Due to a lower (more negative) resting

membrane potential

More severe hypokalemia: progressive weakness,

hypoventilation (due to respiratory muscle

involvement), and eventually complete paralysis.

Sxs seldom occur unless plasma K conc is < 3 mmol/L

Diagnosis

Pseudohypokalemia

o Marked leukocytosis (e.g. AML) low

measured plasma K due to WBC uptake of K at

room temp

o Avoided by storing blood sample on ice or

rapidly separating plasma (or serum) from the

cells.

TTKG – ratio of the K conc in the lumen of the CCD to

that in peritubular capillaries or plasma K

Hypokalemia with TTKG greater than 4 suggests renal K

loss due to increased distal K secretion.

Treatment

A decrement of 1 mmol/L in plasma conc (4.0 to 3.0

mmol/L) deficit of 200-400 mmol

Plasma K < 3.0 mmol/L – deficit of < 600 mmol

KCl - – preparation of choice

o Promote more rapid correction of hypokalemia

and metabolic acidosis

KHCO3 and citrate (metabolized to HCO3) tend to

alkalinize px

o More appropriate for hypokalemia assoc with

chronic diarrhea or RTA

Max conc

o Peripheral vein not more than 40 mmol/L

o Central vein not more than 60 mmol/L

Rate of infusion should not exceed 20 mmol/L

HYPERKALEMIA

Plasma K conc > 5.0 mmol/L

Etiology

Increased K intake is rarely the sole cause of hyperK

K adaptation ensures rapid K excretion in response

to increases in dietary consumption.

Pseudohyperkalemia

o K movement out of cells immediately prior to or

following venipuncture

o Contributing factors: prolonged use of torniquet

w/ or w/o repeated fist clenching, hemolysis,

marked leukocytosis or thrombocytosis

o Leukocytosis and thrombocytosis increases K

conc due to release of intracellular K following

clot formation

Clinical Features

Resting membrane potential is related to ratio of ICF

to ECF K conc.

o hyperK – partially depolarized cell membrane

Prolonged depolarization impairs membrane

excitability, manifest as weakness

o May progress to flaccid paralysis and

hypoventilation

Caridac toxicity – most serious effect

o Does not correlate well with plasma K conc

Treatment

Approach depends on the ff:

◦ Degree of hyperkalemia (as determined

by plasma K conc)

◦ Assoc muscular weakness

◦ Changes on the ECG

Potential fatal hyperK rarely occurs unless

plasma K exceeds 7.5 mmol/L

Severe hyperK – emergent tx directed at

◦ Minimizing membrane depolarization

◦ Shifting K into cells

◦ Promoting K loss

Calcium gluconate – decreases membrane

excitability; has no effect in decreasing K

concentration

K shift:

o Insulin – causes K to shift into cells

o Alkali tx w/ IV Na HCO3 – shift K into

cells

o B2-adrenergic agonists – cellular

uptake of K

Removal

Diuretics (loops and thiazides) – renal K

excretion

Cation-exchange resin (Na poysterene

sulfonate) – promotes exchange of Na

for K in the GIT

Dialysis

HYPERCALCEMIA AND HYPOCALCEMIA

Decrease in ECF calcium triggers increase in PTH

secretion

PTH results in increased tubular reabsorption of calcium

by the kidney, resorption of calcium from bone;

stimulates renal 1,25 hydroxyvitamin D3 production

increase intestinal calcium absorption

HYPERCALCEMIA

Clinical Manifestations

Mild hyperCa (up to 11-11.5 mg/dL) – asx

Neuropsch sxs – trouble concentrating, personality

changes, or depression

Other presenting sxs – PUD, nephrolith, increased

fracture risk

Diagnostic Approach

First step in diagnostic evaluation of hyper- or

hypocalcemia is ensure that the alteration in serum

Ca levels is not due to abnormal albumin conc

About 50% of total calcium is ionized and the rest is

bound principally to albumin.

Every 1 g/dL below 4.1 g/dL albumin, add 0.2 mM

(0.8 mg/dL) to total Ca. vice versa for hyperalb

Primary hyperparathyroidism – most common cause

of chronic hyperCa

Malignancy is second most common cause of chronic

hyperCa.

Second step – PTH

E.g., elevated Ca and low phosphorus (as in primary

hyperparathyroidism) what is expected PTH? low,

but if you have inc PTH or inapprop N PTH then think

of primary hyperparathyroidism

Dec PTH in the face of hypercalcemia – consistent

with non-parathyroid mediated hypercalcemia, most

often due to underlying malignancy

Treatment

• Mild asx hyperCa – no immediate tx, mgt should be

dictated by underlying diagnosis

• Symptomatic hypercalcemia

o Volume expansion – since hyperCa invariably

leads to dehydration; 4-6 L of IV saline may be

required over 1st

24 hours

o Drugs that inhibit bone resorption – if there is

increased calcium mobilization from bone

(malignancy, severe hyperparathyroidism)

o zolendronic acid, pamidronate, etidronate

o Glucocorticoids – preferred therapy for patients

with 1,25(OH)2D-mediated hypercalcemia

o Decrease 1,25(OH)2D production

o IV hydrocortisone, oral prednisone

HYPOCALCEMIA

Suppressed (or “inappropriately low”) PTH level in

the setting of hypocalcemia establishes absent or

reduced PTH secretion (hypoparathyroidism) as the

cause of hypocalcemia.

Elevated PTH level (secondary hyperparathyroidism)

should direct attention to the vitamin D axis as the

cause of hypocalcemia

Causes of hypocalcemia can be divided into 2, either

a hypoparathyroidism or secondary

hyperparathyroidism.

Hypoparathyroidism – even if low Ca, body cannot

increase PTH

2 hyperpara – persistently inc PTH causing Ca to

remain low

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Clinical Manifestations

Asx if decreases in serum Ca are relatively mild and

chronic

Mod to severe hypoCa assoc with paresthesias

(fingers, toes and circumoral regions); caused by

increased neuromuscular irritability

Chvostek’s sign – twitching of the circumoral

muscles in response to gentle tapping of the facial

nerve just anterior to the ear

Trousseau’s sign – induced by inflation of BP cuff to

20mmHg above the px’s systolic BP for 3 minutes

causing carpal spasm

Severe hypocalcemia can induce seizures,

carpopedal spasm, bronchospasm, laryngospasm,

and prolongation of QT interval

Treatment

Acute sxic hypocalcemia – IV calcium gluconate

Continuing hypocalcemia often require constant IV

infusion of calcium gluconate

Chronic hypocalcemia due to hypopara is treated

with oral calcium supplements and either vitamin D2

or D3 or calcitriol [1,25(OH)2D].

Vitamin D deficiency is best treated with vitamin D

supplementation.

ACIDOSIS AND ALKALOSIS

Normal Acid-Base Homeostasis

Normal arterial pH 7.35-7.45

Henderson-Hasselbach equation

pH = 6.1 + log _ HCO3_ ___ PaCO2 x 0.301

Metabolic acidosis – decrease HCO3, pH will decrease

Respiratory acidosis – increase PaCO2, pH will decrease

Metabolic alkalosis – increase HCO3, pH will increase

Respiratory alkalosis – decrease PaCO2, pH will increase

Normal Acid-Base Homeostasis

Metabolic acidosis/alkalosis – compensation is

regulation of PaCO2 (respiratory)

Respiratory acidosis/alkalosis – compensation is

regulation of HCO3 (metabolic)

METABOLIC ACIDOSIS

High anion gap acidosis

Hyperchloremic non-gap acidosis

ANION GAP (Plasma)

o Unmeasured anions in the plasma

o N 10-12 mmol/L

AG = Na – (Cl + HCO3)

High-anion-gap acidoses

Lactic Acidosis

2 types:

o Type A – secondary to poor tissue perfusion

o Type B – aerobic disorders

Tx: Correct underlying condition that disrupts lactate

metabolism

o Type A – circulatory insufficiency (shock, cardiac

failure), severe anemia, mitochondrial enzyme

defects, and inhibitors (carbon monoxide,

cyanide)

o Type B – malignancies, nucleoside analogue

reverse transcriptase inhibitors in HIV, DM,

renal or hepatic failure, thiamine deficiency,

severe infections (cholera, malaria), seizures, or

drug toxins (biguanides, ethanol, methanol,

propylene glycol, isoniazid, and fructose)

13

Diabetic Ketoacidosis

Cause: increased fatty acid metabolism and

accumulation of ketoacids

Occurs in insulin-dependent DM in association with

cessation of insulin or intercurrent illness

Intercurrent illness – infection, gastroenteritis,

pancreatitis, or MI, increases insulin requirements

temporarily and acutely

Volume expansion with isotonic saline if patient is

dehydrated.

Mainstay of tx is IV regular insulin.

Alcoholic Ketoacidosis

Chronic alcoholics abrupt cessation of alcohol

consumption with poor nutrition

Assoc. with binge drinking, vomiting, abdominal

pain, starvation, and volume depletion

Mixed acid-base disorders are common:

hypoperfusion may enhance lactic acid production

Chronic respiratory alkalosis accompany liver disease

Metabolic alkalosis can result from vomiting.

Treatment: correction of extracellular fluid deficits

with IV saline and glucose

Correction of hypophosphatemia, hypokalemia and

hypomagnesemia

Drug- and Toxin-induced Acidosis

Salicylates

Ethylene glycol

Methanol

Isopropyl alcohol

Salicylate-induced Acidosis

Respiratory alkalosis

Mixture of high-AG metabolic acidosis and

respiratory alkalosis

Treatment: vigorous gastric lavage with isotonic

saline immediately followed by administration of

activated charcoal per NG tube

In acidotic patient, IV NaHCO3 is given to alkalinize

urine (urine pH > 7.5)

In presence of renal failure, hemodialysis can be

performed.

Ethylene glycol-induced Acidosis

Commonly used in antifreeze

Ingestion leads to metabolic acidosis and severe

damage to the CNS, lungs, heart, and kidneys

Diagnosis is facilitated by recognizing oxalate crystals

in the urine, the presence of an osmolar gap in

serum, and a high-AG acidosis.

Treatment includes institution of saline or osmotic

diuresis, thiamine and pyridoxine supplements,

fomepizole or ethanol, and hemodialysis.

Methanol-induced Acidosis

Wood alcohol

Treatment is similar to ethylene glycol intoxication.

Isopropyl Alcohol Toxicity

Ingested isopropanol is absorbed rapidly and may be

FATAL when as little as 150 mL is consumed.

Rubbing alcohol, solvent, or de-icer

Treatment: watchful waiting and supportive therapy

Vasopressors if patient is hypotensive, mechanical

ventilation

Renal Failure

Reduced rate of NH4 production and excretion,

primarily die to decreased renal mass.

Renal failure require oral alkali replacement to

maintain HCO3 between 20 and 24 mmol/L.

Hyperchloremic (nongap) metabolic acidosis

14

METABOLIC ALKALOSIS

Often accompanied by hypochloremia and

hypokalemia

Treatment Primarily directed at correcting the underlying

stimulus for HCO3 generation. Remove the factors that sustain the inappropriate in

HCO3 reabsorption NaCl therapy -is usually sufficient to reverse the

alkalosis if ECFV contraction is present, as indicated by low urine Cl.

Respiratory acidosis

Treatment

Depends on its severity and rate of onset

Acutundere resp acidosis can be life-threatening

Measures to reverse the underlying cause should be

undertaken

Simultaneously with restoration of adequate

alveolar ventilation

Respiratory Alkalosis

Treatment

Directed toward alleviation of underlying disorder

End of Transcription

Sorry di ko na carry hanggang abnormalities of urine

volume lang ung napakinggan ko kasi kailangan ko ng

mag-aral at ang toxic ni doc..nagjump sya ng bongga.

Anyways, most naman e nasa ppt nya..but if u need to

clarify anything, nasa Harrison’s Chapter 44 to 46. God

bless!!

15