Crysis Hypertension - Urgency VS Emergency Hypertension

Hypertensive Crisis - Urgency VS Emergency

Introduction

Hypertensive Crisis is typically defined as Systolic Blood Pressure (SBP) > 220 mm Hg or Diastolic BP > 125 mm Hg. Basically, it was devided into 2 types :

• Hypertensive Urgencies
  
• Hypertensive Emergencies
  

Hypertensive Urgency

Hypertensive Urgency are situations in which Blood Pressure must be reduced within a few hours (<> 220 mmHg or DBP > 125 mmHg that persists after a period of observation) and without evidence of acute end-organ damage.

Hypertensive Emergency

Hypertensive Emergency are situations in which SBP > 220 mmHg or DBP > 125 mmHg and require substantial reduction of blood pressure within 1 hour to avoid the risk of serious morbidity or death.

Clinical Manifestation of Hypertensive Emergency :

• Eyes: Retinal hemorrhages and exudates, papilledema.
• CNS: Intracranial hemorrhage, lacunar infarcts, stroke, or hypertensive encephalopathy. The latter is characterized by the insidious onset of headache (often occipital and worse in the morning), nausea, and vomiting, followed by alterations in mental status, lethargy, and restlessness/agitation. Can progress to seizures and coma if untreated. Generally characterized by the lack of localizing neurologic signs.
• CV: Pulmonary edema, unstable angina/myocardial infarction, acute aortic dissection.
• Renal: Malignant nephrosclerosis, leading to acute renal failure, hematuria, and proteinuria. Activation of the renin-angiotensin system can further exacerbate the HTN.
• Hematologic: Hemolytic anemia can occur with severe HTN.

Others Type Of Hypertensive Emergency :

• Malignant Hypertension - In order to diagnose Malignant Hypertension, papilledema must be present
• Accelerated Hypertension - Defined as a recent significant increase over baseline blood pressure that is associated with target organ damage. This is usually vascular damage on funduscopic examination, such as flame-shaped hemorrhages or soft exudates, but without papilledema.
  

Treatment

Hypertensive Urgency

• Goal : To relieve symptoms and bring BP to reasonable level within 24–48 hours, aiming for gradual attainment of optimal control over several weeks
• Medication : Clonidine, Captopril, Metoprolol, and Hydralazine are effective oral agents.
• Precautions : Avoid B-Blockers if cocaine use, Avoid angiotensin-converting enzyme (ACE) inhibitors if renal artery stenosis suspected, Avoid short-acting dihydropyridine calcium channel blockers because BP reduction is often precipitous
  

Hypertensive Emergency

• Goal : To reduce mean arterial pressure by 25% in 1–2 h; then to reduce BP to 160/100 mm Hg over next 6–12 h
  
• Medication : Nitroprusside, labetalol, and nitroglycerin are most commonly used intravenously. Fenoldopam, a peripheral dopamine agonist, is also effective
• Precautions : If with ischemic stroke, only treat if BP exceeds 220/120 mm Hg; aim to reduce by only 10–15%, If thrombolytic agents are to be used to treat ischemic stroke, target BP is <>
• ACE inhibitors are specifically indicated in scleroderma crisis

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Mean Arterial Pressure (MAP)

Mean Arterial Pressure (MAP)

Definition

Mean arterial pressure is a term to describe a notional average blood pressure in an individual. It is defined as the average arterial pressure during a single cardiac cycle.

The blood pressure in our body is always changing and it is part of the human physiology. It is very rare that someone's blood pressure is always the same. Because we are always active and we are always doing different things like eating, sitting, standing, walking, breathing, moving around and doing so many other things throughout a day.

Formula

As blood is pumped out of the left ventricle into the arteries, pressure is generated. The mean arterial pressure (MAP) is determined by the Cardiac Output (CO), Systemic Vascular Resistance (SVR), and Central Venous Pressure (CVP) according to the following relationship, which is based upon the relationship between Flow, Pressure and Resistance :

MAP = (CO × SVR) + CVP

Because CVP is usually at or near 0 mmHg, this relationship is often simplified to:

MAP Approx = CO × SVR

Therefore, changes in either CO or SVR will affect MAP. If CO and SVR change reciprocally and proportionately, then MAP will not change. For example, if CO doubles and SVR decreases by one-half, MAP does not change (if CVP = 0). It is important to note that variables found in are all interdependent. This means that changing one variable changes all of the others.

In practice, MAP is not determined by knowing the CO and SVR, but rather by direct or indirect measurements of arterial pressure. From the aortic pressure trace over time, the shape of the pressure trace yields a mean pressure value (geometric mean) that is less than the arithmetic average of the systolic and diastolic pressures as shown to the right.

Why Measuring The MAP?

There are different reasons that mean arterial pressure is taken and recorded. Not all are related to health. The mean arterial pressure is known as part of a couple biological processes that do not show any health problems. When an arterial blood flow goes through the body it is going somewhere that it has in mind. Usually the blood is pumped through the arteries and left in the beds of capillaries that will run across the surface of different organs and give them the nutritional substances that are needed to operate properly.

Perfusion Pressure is Thought to Actually be The Mean Arterial Pressure.
MAP = Perfusion Pressure

For the mean arterial pressure to allow an organ to operate the way that it should, it must be at around 60 mmHg. This is enough for an organ of the average size person as long as it is remains at this spot. If the value falls below the average, it means that there is not enough blood pumping into the organ and this will cause the organ to become ischemic. The result will be tissue damage to the organ. The mean arterial pressure should be checked and calculated on a regular basis. Some health officials check the value of a person's arterial pressure when they check a person's blood pressure. It is just one of the many calculations that have to be made about blood pressure.

Simplyfied Mean Arterial Pressure (MAP) Equation

MAP = [(2 x Diastolic)+Systolic] / 3

Interpretation

• MAP around 70 - 110 : Normal

• MAP of about 60 : Necessary to Perfuse Coronary Arteries, Brain, Kidneys

• MAP less than 60 : Low Perfusion - Will Cause Ischemic Organ and Tissue Damage

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Prothrombin Time (PT) & International Normalize Ration (INR)

Prothrombin Time (PT) & International Normalize Ratio (INR)

Introduction

An INR is useful in monitoring the impact of anticoagulant (“blood thinning”) medicines, such as Warfarin(Coumadin). Patients with atrial fibrillation often take anticoagulant medications to protect against clots that can cause strokes. While taking Warfarin, patients have regular blood tests to monitor their INR. Just as patients know their blood pressure numbers, they also should know their Warfarin (Coumadin) dosage and their INR.

This standarization system was introduced by World Health Organization (WHO) in 1983 to provide a common basis for the interpretation of the PT result independent of the sensivity of the thromboplastin reagen which tends to vary from one manufacturer to another

Normal Result Of Prothombin Time

Although there is some variation depending on the source of the thromboplastin used in the test. (For this reason, laboratories report a normal control value along with patient results.) A prothrombin time within this range indicates that the patient has normal amounts of clotting factors VII and X.

The Normal Prothrombin Time (PT) is 11-15 seconds

Abnormal Results Of Prothombin Time

A prolonged PT time is considered abnormal. The prothrombin time will be prolonged if the concentration of any of the tested factors is 10% or more below normal plasma values. A prolonged prothrombin time indicates a deficiency in any of factors VII, X, V, prothrombin, or fibrinogen.

It may mean that the patient has a vitamin K deficiency, a liver disease, or disseminated intravascular coagulation (DIC). The prothrombin time of patients receiving warfarin therapy will also be prolonged-usually in the range of one and one half to two times the normal PT time. A PT time that exceeds approximately two and a half times the control value (usually 30 seconds or longer) is grounds for concern, as abnormal bleeding may occur.

Formula

INR = Patient PT / Mean Of Normal Patient Range

Interpretation (INR)

• 1.0 : For Healthy People,
• 2.0 - 3.0 : For patients on anticoagulants, or patients with atrial fibrillation,
• 3.0 - 4.0 : For patients with mechanical heart valves.
• > 4.0 : Indicate that blood is clotting too slowly (High Risk For Uncontrolled Bleeding)

The Ideal INR must be individualized for each patient

While the INR reporting format may improve the management of anti-coagulanted patient, the INR inapproriate in three subsets, such as :

1. The System was designed for patient who are stabilized on oral anticoagulant therapy and is not appropriate for those patient who have recently begun their treatment.
2. Patient with liver disease should not be monitored by the INR since they frequently lack circulating factors
3. Patient who are being routinely screened for clotting factors deficiencies.

Food & Drug Effects

Do not take any prescription or nonprescription medicines without first talking to the doctor who tracks your INR test results. Foods high in vitamin K, a natural blood-clotting factor, can alter an INR. Broccoli, lettuce, spinach and liver are all high in vitamin K. Doctors usually encourage patients to include these nutritious foods in a healthy diet. It is important, however, to consume a consistent amount of these foods and not drastically change eating habits. It is important to have follow up blood tests as scheduled by your doctor and to know your Warfarin (Coumadin) dosage and INR.

Many Food & Drugs Can Change The INR such as :
Aspirin, Ibuprofen, Antibiotics, Vitamin K, Brocolli, Lettuce, Spinach, and Birth Control Pills/Progesterone-Estrogen Combination Pills.

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How To Correct Hyponatremia ?

How To Correct Hyponatremia ?

Serum sodium concentration and serum osmolarity normally are maintained under precise control by homeostatic mechanisms involving stimulation of thirst, secretion of antidiuretic hormone (ADH), and renal handling of filtered sodium. Irreparable harm can befall the patient when abnormal serum sodium levels are corrected too quickly or too slowly.

Classification

• Mild Hyponatremia - Na 135-130mEq/L,
• Moderate Hyponatremia - Na 129-125mEq/L,
• Severe Hyponatremia - Na 124-120mEq/L
  
• Life Threatening - Na <>

Prehospital Care

Prehospital treatment is directed toward treatment of symptoms (eg, seizures, arrhythmias) in severely symptomatic patients; the underlying hyponatremia is unlikely to be recognized prior to evaluation in the ED.

Emergency Department Care

Formulas for the dose and rate of hypertonic saline are based on a sodium deficit and have not been prospectively studied. These formulas should only be used as a guideline, requiring frequent retesting of serum sodium level.

Administration of 3% NaCl should only be required in patients with severely symptomatic hyponatremia (eg, seizures) or potentially in patients with Serum Sodium Level of less than 110 mEq/L

Total Sodium Deficit

Na Deficit (mEq) = (Desired Na – Measured Na) X 0.6 X (Weight in Kilograms)

Correction of Hyponatremia Using 3% Saline

Volume of 3% Saline (L) = (Na Deficit)/513 mEq Na/L

The rate of correction of Chronic Hyponatremia should not exceed 0.5 mEq/L per hour.
The rate of correction of Acute Hyponatremia should not exceed 1 - 2 mEq/L per hour.

Sodium levels should not be corrected to above 120-130 mEq/L or increase by more than 12 mEq/L per day. However, if necessary, as with a patient with Hyponatremia-Induced Seizure or Agitated Confusion, the initial rate of correction can be rapid, provided that the final rate of correction does not exceed 15 mEq/L per 24 hours.

Time Needed For Hyponatremia Correction

Time Needed for Correction = (Desired Na – Measured Na)/0.5 mEq/L per hour

The Rate of Infusion of Hypertonic Saline

Rate = (Volume of 3% Saline)/(Time Needed for Correction)

Other Solution That Can Be Used

Lactated Ringers : Contains 130 mEq/L = 0.130 mEq/ml
0.9% NaCl : Contains 154 mEq/L = 0.154 mEq/ml
1.8% NaCl : Contains 380 mEq/L = 0.380 mEq/ml
3% NaCl : Contains 513 mEq/L = 0.513 mEq/ml

Other Concern

1. Stop therapy when serum sodium concentration approaches 120-130 mEq/L, symptoms resolve, or serum sodium concentration has increased by 15 mEq/L in 24 hours or less.
2. Furosemide increases excretion of free water and can be used (1 mg/kg) in conjunction with isotonic or hypertonic saline.
3. Once normal renal function is ascertained, try to normalize potassium levels prior to or concurrently with the correction of hyponatremia.
4. Monitor serum and urine electrolyte levels. Initially, recheck them in 2 hours, then at least every 4 hours until the patient's levels are stabilized.
5. Aggressive treatment of hyponatremia should always be weighed against the risk of inducing Osmotic Central Pontine Myelinolysis (CMP) / Osmotic Demyelination Syndrome.
   
6. Although rare, osmotic myelinolysis is a serious complication and can develop one to several days after aggressive treatment of hyponatremia. Typical features are Disorders of Upper Motor Neurons including Spastic Quadriparesis and Pseudobulbar Palsy, and Mental Disorders ranging from Confusion to Coma. The risk is increased in persons with hepatic failure, potassium depletion, large burns, and malnutrition.

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Classification Of Acute Renal Failure (Based On The Causes)

Classification Of Acute Renal Failure (Based On The Causes)

The causes of acute renal failure (ARF) are conventionally and conveniently divided into 3 categories : prerenal, renal, and postrenal.

• Prerenal ARF involves an essentially normal kidney that is responding to hypoperfusion by decreasing the glomerular filtration rate (GFR).

• Renal or intrinsic ARF refers to a condition in which the pathology lies within the kidney itself.

• Postrenal ARF is caused by an obstruction of the urinary tract. Acute tubular necrosis (ATN) is the most common cause of ARF in the renal category.

Prerenal ARF

Prerenal ARF represents the most common form of kidney injury and often leads to intrinsic ARF if it is not promptly corrected.

• Volume loss from GI, renal, cutaneous (eg, burns), and internal or external hemorrhage can result in this syndrome.

• Prerenal ARF can also result from decreased renal perfusion in patients with heart failure or shock (eg, sepsis, anaphylaxis).

• Special classes of medications that can induce prerenal ARF in volume-depleted states are angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs), which are otherwise safely tolerated and beneficial in most patients with chronic kidney disease.

• Arteriolar vasoconstriction leading to prerenal ARF can occur in hypercalcemic states, with the use of radiocontrast agents, nonsteroidal anti-inflammatory drugs (NSAIDs), amphotereicin, calcineurin inhibitors, norepinephrine, and other pressor agents.

• The hepatorenal syndrome can also be considered a form of prerenal ARF because functional renal failure develops from diffuse vasoconstriction in vessels supplying the kidney.

Renal or Intrinsic ARF

Structural injury in the kidney is the hallmark of Renal or Intrinsic ARF, and the most common form is acute tubular injury (ATN), either Ischemic or Cytotoxic. Frank necrosis is not prominent in most human cases of ATN and tends to be patchy.

• Intrarenal Vasoconstriction is the dominant mechanism for the reduced glomerular filtration rate (GFR) in patients with ATN. The mediators of this vasoconstriction are unknown, but tubular injury seems to be an important concomitant finding.
  

• Urine backflow and intratubular obstruction (from sloughed cells and debris) are causes of reduced net ultrafiltration. The importance of this mechanism is highlighted by the improvement in renal function that follows relief of such intratubular obstruction.
  

• Apart from the increase in basal renal vascular tone, the stressed renal microvasculature is more sensitive to potentially vasoconstrictive drugs and otherwise-tolerated changes in systemic blood pressure. The vasculature of the injured kidney has an impaired vasodilatory response and loses its autoregulatory behavior.

• A physiologic hallmark of ATN is a failure to maximally dilute or concentrate urine (isosthenuria). This defect is not responsive to pharmacologic doses of vasopressin. The injured kidney fails to generate and maintain a high medullary solute gradient because the accumulation of solute in the medulla depends on normal distal nephron function.
  

• Failure to excrete concentrated urine, even in the presence of oliguria, is a helpful diagnostic clue to distinguish prerenal from intrinsic renal disease, in which urine osmolality is less than 300 mOsm/kg. In prerenal azotemia, urine osmolality is typically more than 500 mOsm/kg.

• Glomerulonephritis can be a cause of ARF and usually falls into a class referred to as rapidly progressive glomerulonephritis (RPGN). The pathologic correlation of RPGN is the presence of glomerular crescents (glomerular injury) on biopsy; if more than 50% of glomeruli contain crescents, this usually results in a significant decline in renal function. Although comparatively rare, acute glomerulonephritides should be part of the diagnostic consideration in cases of ARF.

Postrenal ARF

Mechanical obstruction of the urinary collecting system, including the renal pelvis, ureters, bladder, or urethra, results in obstructive uropathy or postrenal ARF.

• If the site of obstruction is unilateral, then a rise in the serum creatinine level may not be apparent due to contralateral renal function. Although the serum creatinine level may remain low with unilateral obstruction, a significant loss of GFR occurs, and patients with partial obstruction may develop progressive loss of GFR if the obstruction is not relieved. Causes of obstruction include stone disease; stricture; and intraluminal, extraluminal, or intramural tumors.

• Bilateral obstruction is usually a result of prostate enlargement or tumors in men and urologic or gynecologic tumors in women.

• Patients who develop anuria typically have obstruction at the level of the bladder or downstream to it.

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Acute Renal Failure (ARF) - Chronic Renal Insufficiency (CRI) - End Stage Renal Disease (ESRD)

Acute Renal Failure (ARF) VS Chronic Renal Insufficiency (CRI)
VS
End Stage Renal Disease (ESRD)

Acute Renal Failure (ARF)

This is kidney failure that happens rather suddenly, where something has caused the kidneys to shutdown. This may be due to infection, drugs (prescription, over-the-counter, recreational), traumatic injury, major surgery, nephrotoxic poisons, etc.

Emergency dialysis may be needed until the situation resolves and the kidneys begin functioning again (this might take a short time, or months, or it might be permanent). While more acute episodes are possible in the case of IgAN (we often refer to them as "flare-ups"), IgA nephropathy is a condition that mainly causes chronic renal insufficiency (CRI), not usually acute renal failure (ARF).

However, some people may experience spontaneously-reversing acute renal failure as well. The latter are cases where serum creatinine goes up dramatically but later returns to a more normal baseline. In such cases, dialysis may be needed until the condition improves. ARF in the context of IgAN is usually more associated with the person developing a flare-up of HSP.

Chronic Renal Insufficiency (CRI)

This is when a disease such as IgA nephropathy slowly and gradually destroys the filtering capacity of the kidneys. It is sometimes referred to as Progressive Renal Insufficiency, Chronic Kidney Disease or Chronic Renal Failure (CRF). This kind of damage cannot currently be repaired, and as such, it is Irreversible. A person may have chronic renal failure for many years, even decades, before dialysis or a kidney transplant become necessary.

Chronic renal insufficiency does not, by itself, mean complete shutdown of the kidneys, and a person with chronic renal insufficiency may still pass urine normally, and may have more than enough kidney function left for normal functioning of the body. Note that you cannot judge the efficiency of your kidneys by the amount of urine you produce. People with quite advanced renal insufficiency, and even people on dialysis may still produce a fair amount of urine. But this does not mean that the kidneys are filtering waste nor regulating serum electrolyte levels efficiently.

Chronic renal insufficiency itself causes more loss of kidney function. One important aspect of kidney disease is that, once a kidney is damaged by it to a certain degree, it continues to deteriorate even if the underlying kidney disease can or could be cured. This is commonly referred to as the Point of No Return (PNR).

Classification Of Chronic Renal Insufficiency

Early Chronic Renal Insufficiency (Stages 1 to 2)
Advanced Chronic Renal Insufficiency (Stages 3 to 4)

Late Chronic Renal Insufficiency (Stages 5) - ESRD

What happens is that the chronic renal insufficiency (CRI) continues to progress on its own, scarring of the glomeruli continues, and kidney function continues to gradually decline. It's possible that controlling blood pressure with an ACE inhibitor like Ramipril, or an Angiotensin II Receptor Blocker like Cozaar or Avapro may slow this progression of chronic renal insufficiency.

There is also beginning to be some evidence that the class of anti-cholesterol drugs called "Statins" (like Lipitor, for example) may help slow progression of CRI.

The point of no return is generally considered to be when serum creatinine reaches 2.0 mg/dl in U.S. measurements, or about 175 umol/L in international SI measurement.

End-Stage Renal Disease (ESRD)

As Chronic Renal Insufficiency continues and progresses, the person may eventually reach the point where it is considered to be End-Stage Renal Disease (ESRD) also known as Late Chronic Renal Insufficiency. It is at this stage that you are on the threshold of needing renal replacement therapy (any form of dialysis, or a kidney transplant).

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Chronic Kidney Disease Staging

CHRONIC KIDNEY DISEASE STAGING

Introduction

Chronic kidney disease occur whenever the glomerular filtration rate (GFR) is less than 60 mL/min/1.73 m2 for about 3 months, with or without kidney damage, for examples : pathologic abnormalities or markers of damage including (proteinuria or kidney stones).

Classification - Staging

There are five stages of chronic kidney disease based on the GFR (Cockcroft-Gault Formula) :

* Stage 1: Normal or increased GFR (>= 90 mL/min/1.73m2) with evidence of kidney damage.

The emphasis is on diagnosis, treatment and prevention of disease progression.

* Stage 2: Mildly decreased GFR (60-89 mL/min/1.73m2) with evidence of kidney damage.

There is still interest in diagnosis and treatment of the underlying cause but the emphasis is shifting towards prevention of disease progression.

* Stage 3: Moderately decreased GFR (30-59 mL/min/1.73m2).

The emphasis is still on preventing disease progression but the evaluation and treatment of complications are becoming more of an issue.

* Stage 4: Severely decreased GFR (15-29 mL/min/1.73m2).

The emphasis is generally on treating complications and preparing for dialysis or kidney transplantation.

* Stage 5: Very little GFR left (<15 ml/min/1.73m2).

Treating complications becomes increasingly difficult and dialysis is usually started at this point.

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The Cockcroft-Gault Formula - Creatinine Clearance Estimation (By Using GFR)

The Cockcroft-Gault Formula - Creatinine Clearance Estimation
(By Using GFR)

INTRODUCTION

The formula gives the Glomerular Filtration Rate, in ml/hour. In other words, it estimates the rate at which plasma ultrafiltrate is produced by the kidneys.

This is a quick and dirty estimate, and gives a good estimate only when creatinine clearance is stable. If the creatinine concentration is rising, applying this formula would be highly inaccurate.

For most purposes, however, the Cockcroft-Gault formula is the most common formula used by physicians to estimate creatinine clearance, and thus Glomerular Filtration Rate (ml/min/1.73 m2).

THE FORMULA

The Cockcroft-Gault Formula is Used to calculate Creatinine Clearance.

MEN : GFR = (140 - age) x Weight (kg) / (72 x serum creatinine(mg/dl)) X 1

WOMEN : GFR = (140 - age) x Weight (kg) / (72 x serum creatinine(mg/dl)) X 0.85

OR

MEN : GFR = (140 - age) x Weight (kg) / (72 x serum creatinine/88.6(mcmol/L)) X 1

WOMEN : GFR = (140 - age) x Weight (kg) / (72 x serum creatinine/88.6(mcmol/L)) X 0.85

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Naproxen Test

NAPROXEN TEST

Requirement

The patients were given Naproxen Sodium at 500 mg/tablet, one tablet every 12 hours p.c. for a total of 4 doses. Body temperature was taken orally every two hours prior.

Naproxen 500 mg/tablet Every 12 Hours P.C For 2 Days

Interpretation

Fever lysis after or within the time frame of drug administration was interpreted as suggestive of either a neoplastic condition or a connective tissue disease.
Nonresponse of the fever to the drug was taken to suggest an infectious condition.

Naproxen Administration was discontinued if any of the following were noted :

1). Hypersensitivity reaction,
2). Abdominal complaints, or
3). Patient refusal to take the drug.

Pathophysiology

Postulated pathogenic mechanisms for its occurrence include massive tumor necrosis, extensive neoplastic cell destruction, local inflammation due to ulceration of normal or malignant tissue, leucocytic infiltration of the neoplasm, interference with conjugation of pyrogenic steroids secondary to liver metastases and excessive heat production by tumor cells.

Neoplastic Fever is the second most common cause of fever in cancer patients after infection. The establishment of the etiology of fever in patients with malignancy however, remains to be a challenging diagnostic scenario for clinicians. Distinguishing between infectious fever and neoplastic fever is of paramount importance in cancer patients because of the urgency and necessity for appropriate treatment in these immunocompromised hosts.

The more recent mechanism involves induction of pyrogenic cytokines such as tumor necrosis factor, interleukins 1 and 6 and interferon by the tumor cells itself or by host macrophages in response to the tumor. Cytokines stimulate production of prostaglandin E2 which act on the hypothalamus causing a change in the thermostatic set point. Naproxen is a non-steroidal anti-inflammatory drug which acts as an inhibitor of cyclooxygenase. It has been demonstrated to have both analgesic and antipyretic effects.

Subsequent observational studies on small groups of patients with specific malignancies similarly
had promising results, but likewise suffered from this critical flaw. This precluded further estimation of the sensitivity, specificity and likelihood ratios of the naproxen test. It is suggested that the more appropriate reference standard would be the absence of infection after extensive and thorough laboratory work-up coupled with the absence of any clinical deterioration without administration of any antibiotics on continued follow-up for at least a period of 2 weeks. Specifically, the more convincing evidence that a patient does not have any infection despite extensive work-up would be the non-deterioration of the patient in the absence of any antibiotics during a prolonged follow-up period.

With the advent of modern diagnostic technology, it is timely that the usefulness of this
test be re-evaluated in the present decade. In the Philippines, it is best that this test be validated in a tertiary center with a laboratory and radiology department that is equipped with highly sensitive diagnostic and imaging procedures that are needed to rule out any infection from bacterial, viral, fungal or parasitic etiology. Likewise the staff should be competent in the performance and interpretation of these procedures.

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Creatinine and Creatinine Clearance

Creatinine and Creatinine Clearance

Creatinine and creatinine clearance tests measure the level of the waste product creatinine in your blood and urine. These tests tell how well your kidneys are working. The substance creatine is formed when food is changed into energy through a process called metabolism. Creatine is broken down into another substance called creatinine, which is taken out of your blood by the kidneys and then passed out of your body in urine.

Creatinine is made at a steady rate and is not affected by diet or by normal physical activities. If your kidneys are damaged and cannot work normally, the amount of creatinine in your urine goes down while its level in your blood goes up.

Three types of tests on creatinine can be done:

Blood Creatinine Level

The blood creatinine level shows how well your kidneys are working. A high creatinine level may mean your kidneys are not working properly. The amount of creatinine in the blood depends partly on the amount of muscle tissue you have; men generally have higher creatinine levels than women.

Creatinine Clearance Test

A creatinine clearance test measures how well creatinine is removed from your blood by your kidneys. A creatinine clearance test gives better information than a blood creatinine test on how well your kidneys are working. A creatinine clearance test is done on both a blood sample and on a sample of urine collected over 24 hours (24-hour urine sample).

Blood Urea Nitrogen-to-Creatinine ratio (BUN:creatinine)

The levels of blood creatinine and blood urea nitrogen (BUN) can be used to find the BUN-to-creatinine ratio. A BUN-to-creatinine ratio can help your doctor check for problems, such as dehydration, that may cause abnormal BUN and creatinine levels.

Urea is a waste product made when protein is broken down in your body. Urea is made in the liver and passed out of your body in the urine. A blood urea nitrogen (BUN) test measures the amount of urea in your blood. Like creatinine, it can help your doctor see how well your kidneys are working.

Why It Is Done?

A blood creatinine level or a creatinine clearance test is done to:

* See if your kidneys are working normally.
* See if your kidney disease is changing.
* See how well the kidneys work in people who take medicines that can cause kidney damage.
* See if severe dehydration is present. Dehydration generally causes BUN levels to rise more than creatinine levels. This causes a high BUN-to-creatinine ratio. Kidney disease or blockage of the flow of urine from your kidney causes both BUN and creatinine levels to rise.

How To Prepare?

Do not do any strenuous exercise for 2 days (48 hours) before having creatinine tests.

Do not eat more than 8oz of meat, especially beef, or other protein for 24 hours before the blood creatinine test and during the creatinine clearance urine test.

It is important to drink enough fluids during the 24-hour urine collection but do not drink coffee and tea. These are diuretics that cause your body to pass more urine.

Collection of The Blood Sample & The 24-Hour Urine Sample

* Blood Sample will be taken by the Medical Proffesional - then will be examined in the Laboratory for the Blood Creatinin Level.
* After that, you can start collecting your urine in the next morning. When you first get up, empty your bladder but do not save this urine. Write down the time that you urinated to mark the beginning of your 24-hour collection period.
* For the next 24 hours, collect all your urine. Your doctor or lab will usually provide you with a large container that holds about 1 gal (4 L). The container has a small amount of preservative in it. Urinate into a small, clean container and then pour the urine into the large container. Do not touch the inside of the container with your fingers.
* Keep the large container in the refrigerator for the 24 hours.
* Empty your bladder for the final time at or just before the end of the 24-hour period. Add this urine to the large container and record the time.
* Do not get toilet paper, pubic hair, stool (feces), menstrual blood, or other foreign matter in the urine sample.

Results

Creatinine and Creatinine Clearance Tests measure Creatinine Levels in your Blood and Urine to give information about how well your kidneys are working. The creatinine clearance value is found from the amounts of creatinine in the urine and blood and from the amount of urine you pass in 24 hours. This value is the amount of blood cleared of creatinine per minute, based on your body size. Below are the normal range of the Blood Creatinine, Creatinine Clearance & BUN To Creatinin Ratio :

Blood Creatinine:

Men : 0.6–1.2 milligrams per deciliter (mg/dL) or 53-106 micromoles/L (mcmol/L)
Women : 0.5–1.1 mg/dL or 44–97 mcmol/L
Teen 0.5–1.0 mg/dL
Child 0.3–0.7 mg/dL
Newborn 0.3–1.2mg/dL

Creatinine Clearance:

Men 90–140 milliliters per minute (mL/min) or 1.78–2.32 milliters per second (mL/sec)
Women 87–107 mL/min or 1.45-1.78 mL/sec
Creatinine clearance values normally go up as you get older (normal values go down by 6.5 mL/min for every 10 years past the age of 20).

BUN-To-Creatinine Ratio

Over 12 months of age: 10:1–20:1

Infants less than 12 months of age: Up to 30:1

INTERPRETATION

High values

* High creatinine blood levels. High creatinine blood levels can mean serious kidney damage or disease is present. Kidney damage can be caused by a life-threatening infection, shock, cancer, or low blood flow to the kidneys. Other conditions that can cause high blood creatinine levels include blockage of the urinary tract (such as by a kidney stone), heart failure, dehydration, excessive blood loss that causes shock, gout, or muscle conditions (such as rhabdomyolysis, gigantism, acromegaly, myasthenia gravis, muscular dystrophy, and polymyositis). Usually a high blood creatinine level means that the creatinine clearance value is lower than normal.
* High creatinine clearance. High creatinine clearance values can be caused by strenuous exercise, muscle injury (especially crushing injuries), burns, carbon monoxide poisoning, hypothyroidism, and pregnancy.
* High BUN-to-creatinine ratio. High BUN-to-creatinine ratios occur with sudden (acute) kidney failure, which may be caused by shock or severe dehydration. A blockage in the urinary tract (such as a kidney stone) can cause a high BUN-to-creatinine ratio. A very high BUN-to-creatinine ratio may be caused by bleeding in the digestive tract or respiratory tract.

Low Values

* Low blood creatinine levels. Low blood creatinine levels can mean lower muscle mass caused by a disease, such as muscular dystrophy, or by aging. Low levels can also mean some types of severe liver disease or a diet very low in protein. Pregnancy can also cause low blood creatinine levels.
* Low creatinine clearance. Low creatinine clearance levels can mean serious kidney damage is present. Kidney damage can be from conditions such as a life-threatening infection, shock, cancer, low blood flow to the kidneys, or urinary tract blockage. Other conditions, such as heart failure, dehydration, and liver disease (cirrhosis), can also cause low creatinine clearance levels.
* Low BUN-to-creatinine ratio A low BUN-to-creatinine ratio may be associated with a diet low in protein, a severe muscle injury called rhabdomyolysis, pregnancy, cirrhosis, or syndrome of inappropriate antidiuretic hormone secretion (SIADH). SIADH sometimes occurs with lung disease, cancer, diseases of the central nervous system, and the use of certain medications.

What Affects the Test

Reasons you may not be able to have the test or why the results may not be helpful include:

* Taking medicines, such as methyldopa (Aldomet), trimethoprim (Proloprim, Trimpex), vitamin C (ascorbic acid), cimetidine (Tagamet), some diuretics, and cephalosporin antibiotics, especially cefoxitin (Mefoxin). These affect the blood creatinine levels.
* Taking medicines, such as vitamin C (ascorbic acid), phenytoin (Dilantin), some cephalosporin antibiotics, captopril, aminoglycosides (Garamycin), trimethoprim (Proloprim, Trimpex), cimetidine (Tagamet), quinine, quinidine (Cardioquin, Quinaglute, Quinidex), procainamide, and the antifungal medication amphotericin B. These affect the creatinine clearance levels.
* Taking medicines, such as cimetidine (Tagamet), steroids, and tetracycline antibiotics. These can affect the BUN-to-creatinine ratio.
* Doing strenuous exercise 2 days before creatinine clearance test.
* Eating more than 8oz of meat, especially beef, in the 24 hours before a blood creatinine test and during a creatinine clearance urine test.

What To Think About

* A high blood creatinine level is generally seen with a low creatinine clearance level because creatinine in the blood is removed by the kidneys. If the kidneys are not able to remove creatinine (low creatinine clearance), levels of creatinine in the blood go up (high blood creatinine level).
* If you are pregnant, your doctor can check the amount of creatinine in amniotic fluid to see how developed, or mature, your baby's kidneys are. This can be helpful if there is a chance your baby will be delivered early. A baby who has mature kidneys will make more creatinine than a baby whose kidneys are still developing.
* A normal blood creatinine level does not rule out kidney disease. To help see whether kidney damage may be present, a BUN level is also measured. Other tests may also be done to check for kidney disease. For more information, see the medical test Blood Urea Nitrogen.
* Creatinine levels increase more slowly than blood urea nitrogen (BUN) levels, so an increase in creatinine may mean chronic kidney problems.
* A glomerular filtration rate may be done for people with chronic kidney disease to regularly check how well the kidneys are working.
* Diabetes experts recommend that blood creatinine levels be done every year for people with diabetes. The creatinine level is used to find the glomerular filtration rate, which shows how well the kidneys are working.
* The amount of creatinine in the blood depends partly on the amount of muscle tissue; blood creatinine levels are generally higher in men than in women. Also, people who have large muscles, such as athletes, normally have above-average blood creatinine levels.
* A one-time urine sample to measure urine creatinine and sodium is sometimes done along with blood creatinine and sodium levels to help find the fractional excretion of sodium (FENA). This test can help your doctor see whether a problem with blood flow to the kidneys is caused by dehydration or shock or by damage to the kidneys themselves.

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