ROLE OF LABORATORY TESTS IN DIABETES MELLITUS Featured

Written by 
Published in Clinical Pathology
Thursday, 17 August 2017 21:35
Rate this item
(1 Vote)
In DM, applications of laboratory tests are as follows:
 
  • Diagnosis of DM
  • Screening of DM
  • Assessment of glycemic control
  • Assessment of associated long-term risks
  • Management of acute metabolic complications.
 
LABORATORY TESTS FOR DIAGNOSIS OF DIABETES MELLITUS
 
Diagnosis of DM is based exclusively on demonstration of raised blood glucose level (hyperglycemia).
 
The current criteria (American Diabetes Association, 2004) for diagnosis of DM are as follows:
 
Typical symptoms of DM (polyuria, polydipsia, weight loss) and random plasma glucose ≥ 200 mg/dl (≥ 11.1 mmol/L)
 
Or
 
Fasting plasma glucose ≥ 126 mg/dl (≥ 7.0 mmol/L)
 
Or
 
2-hour post glucose load (75 g) value during oral glucose tolerance test ≥ 200 mg/dl (≥ 11.1 mmol/L).
 
If any one of the above three criteria is present, confirmation by repeat testing on a subsequent day is necessary for establishing the diagnosis of DM. However, such confirmation by repeat testing is not required if patient presents with (a) hyperglycemia and ketoacidosis, or (b) hyperosmolar hyperglycemia.
 
The tests used for laboratory diagnosis of DM are (1) estimation of blood glucose and (2) oral glucose tolerance test.
 
Estimation of Blood Glucose
 
Measurement of blood glucose level is a simple test to assess carbohydrate metabolism in DM (Figure 837.1). Since glucose is rapidly metabolized in the body, measurement of blood glucose is indicative of current state of carbohydrate metabolism.
 
Figure 837.1 Blood glucose values in normal individuals
Figure 837.1 Blood glucose values in normal individuals, prediabetes, and diabetes mellitus
 
Glucose concentration can be estimated in whole blood (capillary or venous blood), plasma or serum. However, concentration of blood glucose differs according to nature of the blood specimen. Plasma glucose is about 15% higher than whole blood glucose (the figure is variable with hematocrit). During fasting state, glucose levels in both capillary and venous blood are about the same. However, postprandial or post glucose load values are higher by 20-70 mg/dl in capillary blood than venous blood. This is because venous blood is on a return trip after delivering blood to the tissues.
 
When whole blood is left at room temperature after collection, glycolysis reduces glucose level at the rate of about 7 mg/dl/hour. Glycolysis is further increased in the presence of bacterial contamination or leucocytosis. Addition of sodium fluoride (2.5 mg/ml of blood) maintains stable glucose level by inhibiting glycolysis. Sodium fluoride is commonly used along with an anticoagulant such as potassium oxalate or EDTA. Addition of sodium fluoride is not necessary if plasma is separated from whole blood within 1 hour of blood collection.
 
Plasma is preferred for estimation of glucose since whole blood glucose is affected also by concentration of proteins (especially hemoglobin).
 
There are various methods for estimation of blood glucose:
 
  • Chemical methods:
    – Orthotoluidine method
    – Blood glucose reduction methods using neocuproine, ferricyanide, or copper.
 
Chemical methods are less specific but are cheaper as compared to enzymatic methods.
 
  • Enzymatic methods: These are specific for glucose.
    – Glucose oxidase-peroxidase
    – Hexokinase
    – Glucose dehydrogenase
 
Chemical methods have now been replaced by enzymatic methods.
 
Terms used for blood glucose specimens: Depending on the time of collection, different terms are used for blood glucose specimens.
 
  • Fasting blood glucose: Sample for blood glucose is withdrawn after an overnight fast (no caloric intake for at least 8 hours).
  • Post meal or postprandial blood glucose: Blood sample for glucose estimation is collected 2 hours after the subject has taken a normal meal.
  • Random blood glucose: Blood sample is collected at any time of the day, without attention to the time of last food intake.
 
Oral Glucose Tolerance Test (OGTT)
 
Glucose tolerance refers to the ability of the body to metabolize glucose. In DM, this ability is impaired or lost and glucose intolerance represents the fundamental pathophysiological defect in DM. OGTT is a provocative test to assess response to glucose challenge in an individual (Figure 837.2).
 
Figure 837.2 Oral glucose tolerance curve
Figure 837.2 Oral glucose tolerance curve
 
American Diabetes Association does not recommend OGTT for routine diagnosis of type 1 or type 2 DM. This is because fasting plasma glucose cutoff value of 126 mg/dl identifies the same prevalence of abnormal glucose metabolism in the population as OGTT. World Health Organization (WHO) recommends OGTT in those cases in which fasting plasma glucose is in the range of impaired fasting glucose (i.e. 100-125 mg/dl). Both ADA and WHO recommend OGTT for diagnosis of gestational diabetes mellitus.
 
Preparation of the Patient
 
  • Patient should be put on a carbohydrate-rich, unrestricted diet for 3 days. This is because carbohydrate-restricted diet reduces glucose tolerance.
  • Patient should be ambulatory with normal physical activity. Absolute bed rest for a few days impairs glucose tolerance.
  • Medications should be discontinued on the day of testing.
  • Exercise, smoking, and tea or coffee are not allowed during the test period. Patient should remain seated.
  • OGTT is carried out in the morning after patient has fasted overnight for 8-14 hours.
 
Test
 
  1. A fasting venous blood sample is collected in the morning.
  2. Patient ingests 75 g of anhydrous glucose in 250-300 ml of water over 5 minutes. (For children, the dose is 1.75 g of glucose per kg of body weight up to maximum 75 g of glucose). Time of starting glucose drink is taken as 0 hour.
  3. A single venous blood sample is collected 2 hours after the glucose load. (Previously, blood samples were collected at ½, 1, 1½, and 2 hours, which is no longer recommended).
  4. Plasma glucose is estimated in fasting and 2-hour venous blood samples.
 
Interpretation of blood glucose levels is given in Table 837.1.
 
Table 837.1 Interpretation of oral glucose tolerance test
Parameter Normal Impaired fasting glucose Impaired glucose tolerance Diabetes mellitus
(1) Fasting (8 hr) < 100 100-125 ≥ 126
(2) 2 hr OGTT < 140 < 140 140-199 ≥ 200
 
OGTT in gestational diabetes mellitus: Impairment of glucose tolerance develops normally during pregnancy, particularly in 2nd and 3rd trimesters. Following are the recent guidelines of ADA for laboratory diagnosis of GDM:
 
  • Low-risk pregnant women need not be tested if all of the following criteria are met, i.e. age below 25 years, normal body weight (before pregnancy), absence of diabetes in first-degree relatives, member of an ethnic group with low prevalence of DM, no history of poor obstetric outcome, and no history of abnormal glucose tolerance.
  • Average-risk pregnant women (i.e. who are in between low and high risk) should be tested at 24-28 weeks of gestation.
  • High-risk pregnant women i.e. those who meet any one of the following criteria should be tested immediately: marked obesity, strong family history of DM, glycosuria, or personal history of GDM.
 
Initially, fasting plasma glucose or random plasma glucose should be obtained. If fasting plasma glucose is ≥ 126 mg/dl or random plasma glucose is ≥ 200 mg/dl, repeat testing should be carried out on a subsequent day for confirmation of DM. If both the tests are normal, then OGTT is indicated in average-risk and high-risk pregnant women.
 
There are two approaches for laboratory diagnosis of GDM
 
  • One step approach
  • Two step approach
 
In one step approach, 100 gm of glucose is administered to the patient and a 3-hour OGTT is performed. This test may be cost-effective in high-risk pregnant women.
 
In two-step approach, an initial screening test is done in which patient drinks a 50 g glucose drink irrespective of time of last meal and a venous blood sample is collected 1 hour later (O’Sullivan’s test). GDM is excluded if glucose level in venous plasma sample is below 140 mg/dl. If level exceeds 140 mg/dl, then the complete 100 g, 3-hour OGTT is carried out.
 
In the 3-hour OGTT, blood samples are collected in the morning (after 8-10 hours of overnight fasting), and after drinking 100 g glucose, at 1, 2, and 3 hours. For diagnosis of GDM, glucose concentration should be above the following cut-off values in 2 or more of the venous plasma samples:
 
  • Fasting: 95 mg/dl
  • 1 hour: 180 mg/dl
  • 2 hour: 155 mg/dl
  • 3 hour: 140 mg/dl
 
LABORATORY TESTS FOR SCREENING OF DIABETES MELLITUS
 
Aim of screening is to identify asymptomatic individuals who are likely to have DM. Since early detection and prompt institution of treatment can reduce subsequent complications of DM, screening may be an appropriate step in some situations.
 
Screening for type 2 DM: Type 2 DM is the most common type of DM and is usually asymptomatic in its initial stages. Its onset occurs about 5-7 years before clinical diagnosis. Evidence indicates that complications of type 2 DM begin many years before clinical diagnosis. American Diabetes Association recommends screening for type 2 DM in all asymptomatic individuals ≥ 45 years of age using fasting plasma glucose. If fasting plasma glucose is normal (i.e. < 100 mg/dl), screening test should be repeated every three years.
 
Another approach is selective screening i.e. screening individuals at high risk of developing type 2 DM i.e. if one or more of the following risk factors are presentobesity (body mass index ≥ 25.0 kg/m2), family history of DM (first degree relative with DM), high-risk ethnic group, hypertension, dyslipidemia, impaired fasting glucose, impaired glucose tolerance, or history of GDM. In such cases, screening is performed at an earlier age (30 years) and repeated more frequently.
 
Recommended screening test for type 2 DM is fasting plasma glucose. If ≥126 mg/dl, it should be repeated on a subsequent day for confirmation of diagnosis. If <126 mg/dl, OGTT is indicated if clinical suspicion is strong. A 2-hour post-glucose load value in OGTT ≥200 mg/dl is indicative of DM and should be repeated on a different day for confirmation.
 
Screening for type 1 DM: Type 1 DM is detected early after its onset since it has an acute presentation with characteristic clinical features. Therefore, it is not necessary to screen for type 1 DM by estimation of blood glucose. Detection of immunologic markers (mentioned earlier) has not been recommended to identify persons at risk.
 
Screening for GDM: Given earlier under OGTT in gestational diabetes mellitus.
 
LABORATORY TESTS TO ASSESS GLYCEMIC CONTROL
 
There is a direct correlation between the degree of blood glucose control in DM (both type 1 and type 2) and the development of microangiopathic complications i.e. nephropathy, retinopathy, and neuropathy. Maintenance of blood glucose level as close to normal as possible (referred to as tight glycemic control) reduces the risk of microvascular complications. There is also association between persistently high blood glucose values in DM with increased cardiovascular mortality.
 
Following methods can monitor degree of glycemic control:
 
  • Periodic measurement of glycated hemoglobin (to assess long-term control).
  • Daily self-assessment of blood glucose (to assess day-to- day or immediate control).
 
Glycated Hemoglobin (Glycosylated Hemoglobin, HbA1C)
 
Glycated hemoglobin refers to hemoglobin to which glucose is attached nonenzymatically and irreversibly; its amount depends upon blood glucose level and lifespan of red cells.
 
Hemoglobin + Glucose ↔ Aldimine → Glycated hemoglobin
 
Plasma glucose readily moves across the red cell membranes and is being continuously combined with hemoglobin during the lifespan of the red cells (120 days). Therefore, some hemoglobin in red cells is present normally in glycated form. Amount of glycated hemoglobin in blood depends on blood glucose concentration and lifespan of red cells. If blood glucose concentration is high, more hemoglobin is glycated. Once formed, glycated hemoglobin is irreversible. Level of glycated hemoglobin is proportional to the average glucose level over preceding 6-8 weeks (about 2 months). Glycated hemoglobin is expressed as a percentage of total hemoglobin. Normally, less than 5% of hemoglobin is glycated.
 
Numerous prospective studies have demonstrated that a good control of blood glucose reduces the development and progression of microvascular complications (retinopathy, nephropathy, and peripheral neuropathy) of diabetes mellitus. Mean glycated hemoglobin level correlates with the risk of these complications.
 
The terms glycated hemoglobin, glycosylated hemoglobin, glycohemoglobin, HbA1, and HbA1c are often used interchangeably in practice. Although these terms refer to hemoglobins that contain nonenzymatically added glucose residues, hemoglobins thus modified differ. Most of the studies have been carried out with HbA1c.
 
Glycated hemoglobin should be routinely measured in all diabetic patients (both type 1 and type 2) at regular intervals to assess degree of long-term glycemic control. Apart from mean glycemia (over preceding 120 days), glycated hemoglobin level also correlates with the risk of the development of chronic complications of DM. In DM, it is recommended to maintain glycated hemoglobin level to less than 7%.
 
Box 837.1 Glycated hemoglobin 
  • Hemoglobin A1C of 6% corresponds to mean serum glucose level of 135 mg/dl. With every rise of 1%, serum glucose increases by 35 mg/dl. Approximations are as follows:
    – Hb A1C 7%: 170 mg/dl
    – Hb A1C 8%: 205 mg/dl
    – Hb A1C 9%: 240 mg/dl
    – Hb A1C 10%: 275 mg/dl
    – Hb A1C 11%: 310 mg/dl
    – Hb A1C 12%: 345 mg/dl
  • Assesses long-term control of DM (thus indirectly confirming plasma glucose results or self-testing results).
  • Assesses whether treatment plan is working
  • Measurement of glycated hemoglobin does not replace measurement of day-to-day control by glucometer devices.
Spurious results of glycated hemoglobin are seen in reduced red cell survival (hemolysis), blood loss, and hemoglobinopathies.
 
In DM, if glycated hemoglobin is less than 7%, it should be measured every 6 months. If >8%, then more frequent measurements (every 3 months) along with change in treatment are advocated.
 
There are various methods for measurement of glycated hemoglobin such as chromatography, immunoassay, and agar gel electrophoresis.
 
Role of glycated hemoglobin in management of DM is highlighted in Box 837.1.
 
Self-Monitoring of Blood Glucose (SMBG)
 
Diabetic patients are taught how to regularly monitor their own blood glucose levels. Regular use of SMBG devices (portable glucose meters) by diabetic patients has improved the management of DM. With SMBG devices, blood glucose level can be monitored on day-to-day basis and kept as close to normal as possible by adjusting insulin dosage. SMBG devices measure capillary whole blood glucose obtained by fingerprick and use test strips that incorporate glucose oxidase or hexokinase. In some strips, a layer is incorporated to exclude blood cells so that glucose in plasma is measured. Aim of achieving tight glycemic control introduces the risk of severe hypoglycemia. Daily use of SMBG devices can avoid major hypoglycemic episodes.
 
SMBG devices yield unreliable results at very high and very low glucose levels. It is necessary to periodically check the performance of the glucometer by measuring parallel venous plasma glucose in the laboratory.
 
Portable glucose meters are used by patients for day-to-day self-monitoring, by physicians in their OPD clinics, and by health care workers for monitoring admitted patients at the bedside. These devices should not be used for diagnosis and population screening of DM as they lack precision and there is variability of results between different meters.
 
Goal of tight glycemic control in type 1 DM patients on insulin can be achieved through self-monitoring of blood glucose by portable blood glucose meters.
 
Glycosuria
 
Semiquantitative urine glucose testing for monitoring of diabetes mellitus in home setting is not recommended. This is because (1) even if glucose is absent in urine, no information about blood glucose concentration below the renal threshold (which itself is variable) is obtained (Normally, renal threshold is around 180 mg/dl; it tends to be lower in pregnancy (140 mg/dl) and higher in old age and in long-standing diabetics; in some normal persons it is low), (2) urinary glucose testing cannot detect hypoglycemia, and (3) concentration of glucose in urine is affected by urinary concentration. Semiquantitative urine glucose testing for monitoring has now been replaced by self-testing by portable glucose meters.
 
LABORATORY TESTS TO ASSESS LONG-TERM RISKS
 
Urinary Albumin Excretion
 
Diabetes mellitus is one of the leading causes of renal failure. Diabetic nephropathy develops in around 20-30% of patients with type 1 or type 2 DM. Diabetic nephropathy progresses through different stages as shown in Figure 837.3. Hypertension also develops along the course of nephropathy with increasing albumin excretion. Evidence indicates that if diabetic nephropathy is detected early and specific treatment is instituted, further progression of nephropathy can be significantly ameliorated. Early detection of diabetic nephropathy is based on estimation of urinary albumin excretion. In all adult patients with DM, usual reagent strip test for proteinuria should be carried out periodically. Positive test means presence of overt proteinuria or clinical proteinuria and may be indicative of overt nephropathy. In all such patients quantitation of albuminuria should be carried out to plan appropriate therapy. If the routine dipstick test for proteinuria is negative, test for microalbuminuria should be carried out.
 
Figure 837.3 Evolution of diabetic nephropathy
Figure 837.3 Evolution of diabetic nephropathy. In 80% of patients with type 1 DM, microalbuminuria progresses in 10-15 years to overt nephropathy that is then followed in majority of cases by progressive fall in GFR and ultimately end-stage renal disease. Amongst patients with type 2 DM and microalbuminuria, 20-40% of patients progress to overt nephropathy, and about 20% of patients with overt nephropathy develop end-stage renal disease. Abbreviation: GFR: Glomerular filtration rate
 
The term ‘microalbuminuria’ refers to the urinary excretion of albumin below the level of detection by routine dipstick testing but above normal (30-300 mg/ 24 hrs, 20-200 μg/min, or 30-300 μg/mg of creatinine). Albumin excretion rate is intermediate between normal (normal albumin excretion in urine is < 30 mg/24 hours) and overt albuminuria (> 300 mg/24 hours). Significance of microalbuminuria in DM is as follows:
 
  • It is the earliest marker of diabetic nephropathy. Early diabetic nephropathy is reversible.
  • It is a risk factor for cardiovascular disease in both type 1 and type 2 patients.
  • It is associated with higher blood pressure and poor glycemic control.
 
Specific therapeutic interventions such as tight glycemic control, administration of ACE (angiotensinconverting enzyme) inhibitors, and aggressive treatment of hypertension significantly slow down the progression of diabetic nephropathy.
 
In type 2 DM, screening for microalbuminuria should begin at the time of diagnosis, whereas in type 1 DM, it should begin 5 years after diagnosis. At this time, a routine reagent strip test for proteinuria is carried out; if negative, testing for microalbuminuria is done. Thereafter, in all patients who test negative, screening for microalbuminuria should be repeated every year.
 
Screening tests for microalbuminuria include:
 
 
Reagent strip tests to detect microalbuminuria are available. Positive results should be confirmed by more specific quantitative tests like radioimmunoassay and enzyme immunoassay. For diagnosis of microalbuminuria, tests should be positive in at least two out of three different samples over a 3 to 6 month period.
 
Lipid Profile
 
Abnormalities of lipids are associated with increased risk of coronary artery disease (CAD) in patients with DM. This risk can be reduced by intensive treatment of lipid abnormalities. Lipid parameters which should be measured include:
 
  • Total cholesterol
  • Triglycerides
  • Low-density lipoprotein (LDL) cholesterol
  • High-density lipoprotein (HDL) cholesterol
 
The usual pattern of lipid abnormalities in type 2 DM is elevated triglycerides, decreased HDL cholesterol and higher proportion of small, dense LDL particles. Patients with DM are categorized into high, intermediate and low-risk categories depending on lipid levels in blood (Table 837.2).
 
Table 837.2 Categorization of cardiovascular risk in diabetes mellitus according to lipid levels (American Diabetes Association)
Category Low density lipoproteins High density lipoproteins Triglycerides
High-risk ≥130 < 35 (men) ≥ 400
    < 45 (women)  
Intermediate risk 100-129 35-45 200-399
Low-risk < 100 > 45 (men) < 200
    > 55 (women)  
 
Annual lipid profile is indicated in all adult patients with DM.
 
LABORATORY TESTS IN THE MANAGEMENT OF ACUTE METABOLIC COMPLICATIONS OF DIABETES MELLITUS
 
The three most serious acute metabolic complications of DM are:
 
  • Diabetic ketoacidosis (DKA)
  • Hyperosmolar hyperglycemic state (HHS)
  • Hypoglycemia
 
The typical features of DKA are hyperglycemia, ketosis, and acidosis. The common causes of DKA are infection, noncompliance with insulin therapy, alcohol abuse and myocardial infarction. Patients with DKA present with rapid onset of polyuria, polydipsia, polyphagia, weakness, vomiting, and sometimes abdominal pain. Signs include Kussmaul’s respiration, odour of acetone on breath (fruity), mental clouding, and dehydration. Classically, DKA occurs in type 1, while HHS is more typical of type 2 DM. However, both complications can occur in either types. If untreated, both events can lead to coma and death.
 
Hyperosmolar hyperglycemic state is characterized by very high blood glucose level (> 600 mg/dl), hyperosmolality (>320 mOsmol/kg of water), dehydration, lack of ketoacidosis, and altered mental status. It usually occurs in elderly type 2 diabetics. Insulin secretion is adequate to prevent ketosis but not hyperglycemia. Causes of HHS are illness, dehydration, surgery, and glucocorticoid therapy.
 
Differences between DKA and HHS are presented in Table 837.3.
 
Table 837.3 Comparison of diabetic ketoacidosis and hyperosmolar hyperglycemic state
Parameter Diabetic ketoacidosis Hyperosmolar hyperglycemic state
1. Type of DM in which more common  Type 1 Type 2 
2. Age  Younger age  Older age
3. Prodromal clinical features  < 24 hrs  Several days
4. Abdominal pain, Kussmaul’s respiration  Yes  No
5. Acidosis  Moderate/Severe  Absent
6. Plasma glucose  > 250 mg/dl  Very high (>600 mg/dl)
7. Serum bicarbonate  <15 mEq/L  >15 mEq/L
8. Blood/urine ketones  ++++  ±
9. β-hydroxybutyrate  High  Normal or raised
10. Arterial blood pH  Low (<7.30)  Normal (>7.30)
11. Effective serum osmolality*  Variable  Increased (>320)
12. Anion gap**  >12  Variable
Osmolality: Number of dissolved (solute) particles in solution; normal: 275-295 mOsmol/kg
** Anion gap: Difference between sodium and sum of chloride and bicarbonate in plasma; normal average value is 12
 
Laboratory evaluation consists of following investigations:
 
  • Blood and urine glucose
  • Blood and urine ketone
  • Arterial pH, Blood gases
  • Serum electrolytes (sodium, potassium, chloride, bicarbonate)
  • Blood osmolality
  • Serum creatinine and blood urea.
 
Testing for ketone bodies: Ketone bodies are formed from metabolism of free fatty acids and include acetoacetic acid, acetone and β-hydroxybutyric acid.
 
Indications for testing for ketone bodies in DM include:
 
  • At diagnosis of diabetes mellitus
  • At regular intervals in all known cases of diabetes, during pregnancy with pre-existing diabetes, and in gestational diabetes
  • In known diabetic patients: during acute illness, persistent hyperglycemia (> 300 mgs/dl), pregnancy, and clinical evidence of diabetic acidosis (nausea, vomiting, abdominal pain).
 
An increased amount of ketone bodies in patients with DM indicate impending or established diabetic ketoacidosis and is a medical emergency. Method based on colorimetric reaction between ketone bodies and nitroprusside (by dipstick or tablet) is used for detection of both blood and urine ketones.
 
Test for urine ketones alone should not be used for diagnosis and monitoring of diabetic ketoacidosis. It is recommended to measure β-hydroxybutyric acid (which accounts for 75% of all ketones in ketoacidosis) for diagnosis and monitoring DKA.
 
REFERENCE RANGES
 
  • Venous plasma glucose:
    Fasting: 60-100 mg/dl
    At 2 hours in OGTT (75 gm glucose): <140 mg/dl
  • Glycated hemoglobin: 4-6% of total hemoglobin
  • Lipid profile:
    – Serum cholesterol: Desirable level: <200 mg/dl
    – Serum triglycerides: Desirable level: <150 mg/dl
    – HDL cholesterol: ≥60 mg/dl
    – LDL cholesterol: <130 mg/dl
    – LDL/HDL ratio: 0.5-3.0
  • C-peptide: 0.78-1.89 ng/ml
  • Arterial pH: 7.35-7.45
  • Serum or plasma osmolality: 275-295 mOsm/kg of water.

Serum Osmolality can also be calculated by the following formula recommended by American Diabetes Association:
 
Effective serum osmolality (mOsm/kg) = (2 × sodium mEq/L) + Plasma glucose (mg/dl)
                                                                                                            18
 
  • Anion gap:
    – Na+ – (Cl + HCO3): 8-16 mmol/L (Average 12)
    – (Na+ + K+) – (Cl + HCO3): 10-20 mmol/L (Average 16)
  • Serum sodium: 135-145 mEq/L
  • Serum potassium: 3.5-5.0 mEq/L
  • Serum chloride: 100-108 mEq/L
  • Serum bicarbonate: 24-30 mEq/L
 
CRITICAL VALUES
 
  • Venous plasma glucose: > 450 mg/dl
  • Strongly positive test for glucose and ketones in urine
  • Arterial pH: < 7.2 or > 7.6
  • Serum sodium: < 120 mEq/L or > 160 mEq/L
  • Serum potassium: < 2.8 mEq/L or > 6.2 mEq/L
  • Serum bicarbonate: < 10 mEq/L or > 40 mEq/L
  • Serum chloride: < 80 mEq/L or > 115 mEq/L

Additional Info

  • Reference(s):
    • American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care 2004; 24:S5-S10.
    • American Diabetes Association. Gestational diabetes mellitus. Diabetes Care 2004;27:S88-S90.
    • American Diabetes Association. Hyperglycemic crises in diabetes. Diabetes Care 2004;27:S94-S102.
    • American Diabetes Association. Screening for type 2 diabetes. Diabetes Care 2004;27:S11-S14.
    • American Diabetes Association. Tests of glycemia in diabetes. Diabetes Care 2004;27:S91-S93.
    • Lernmark A. Type 1 diabetes. Clin Chem 1999;45:1331-38.
    • Lebovitz HE. Type 2 diabetes: An overview. Clin Chem 1999;45:1339-45.
    • Reaven GM. The metabolic syndrome: Requiescat in pace. Clin Chem 2005;51:931-8.
    • Reinauer H, Home PD, Kanagasabapathy AS, Heuck C. Laboratory diagnosis and monitoring of diabetes mellitus. Geneva. World Health Organization, 2002.
    • Sacks DB, Bruns DE, Goldstein DE, Maclaren NK, McDonald JM, Parrott M. Guidelines and recommendations for laboratory analysis in the diagnosis and management of diabetes mellitus. Clin Chem 2002; 48:436-72.
    • Trachtenbarg DE. Diabetic ketoacidosis. Am Fam Physician 2005;71:1705-14.
Last modified on Sunday, 27 August 2017 13:40
Dayyal Dg.

Clinical laboratory professional specialized to external quality assessment (proficiency testing) schemes for Laboratory medicine and clinical pathology. | Author/Writer/Blogger

Related items

  • TOTAL THYROXINE (T4)
    Total serum thyroxine includes both free and protein-bound thyroxine and is usually measured by competitive immunoassay. Normal level in adults is 5.0-12.0 μg/dl.
     
    Test for total thyroxine or free thyroxine is usually combined with TSH measurement and together they give the best assessment of thyroid function.
     
    Causes of Increased Total T4
     
    1. Hyperthyroidism: Elevation of both T4 and T3 values along with decrease of TSH are indicative of primary hyperthyroidism.
    2. Increased thyroxine-binding globulin: If concentration of TBG increases, free hormone level falls, release of TSH from pituitary is stimulated, and free hormone concentration is restored to normal. Reverse occurs if concentration of binding proteins falls. In either case, level of free hormones remains normal, while concentration of total hormone is altered. Therefore, estimation of only total T4 concentration can cause misinterpretation of results in situations that alter concentration of TBG.
    3. Factitious hyperthyroidism
    4. Pituitary TSH-secreting tumor.
     
    Causes of Decreased Total T4
     
    1. Primary hypothyroidism: The combination of decreased T4 and elevated TSH are indicative of primary hypothyroidism.
    2. Secondary or pituitary hypothyroidism
    3. Tertiary or hypothalamic hypothyroidism
    4. Hypoproteinaemia, e.g. nephrotic syndrome
    5. Drugs: oestrogen, danazol
    6. Severe non-thyroidal illness.
     
    Free Thyroxine (FT4)
     
    FT4 comprises of only a small fraction of total T4, is unbound to proteins, and is the metabolically active form of the hormone. It constitutes about 0.05% of total T4. Normal range is 0.7 to 1.9 ng/dl. Free hormone concentrations (FT4 and FT3) correlate better with metabolic state than total hormone levels (since they are not affected by changes in TBG concentrations).
     
    Measurement of FT4 is helpful in those situations in which total T4 level is likely to be altered due to alteration in TBG level (e.g. pregnancy, oral contraceptives, nephrotic syndrome).
     
    Total and Free Triiodothyronine (T3)
     
    Uses
     
    1. Diagnosis of T3 thyrotoxicosis: Hyperthyroidism with low TSH and elevated T3, and normal T4/FT4 is termed T3 thyrotoxicosis.
    2. Early diagnosis of hyperthyroidism: In early stage of hyperthyroidism, total T4 and free T4 levels are normal, but T3 is elevated.
     
    A low T3 level is not useful for diagnosis of hypothyroidism since it is observed in about 25% of normal individuals.
     
    For routine assessment of thyroid function, TSH and T4 are measured. T3 is not routinely estimated because normal plasma levels are very low.
     
    Normal T3 level is 80-180 ng/dl.
     
    Free T3: Measurement of free T3 gives true values in patients with altered serum protein levels (like pregnancy, intake of estrogens or oral contraceptives, and nephrotic syndrome). It represents 0.5% of total T3.
     
    Thyrotropin Releasing Hormone (TRH) Stimulation Test
     
    Uses
     
    1. Confirmation of diagnosis of secondary hypothyroidism
    2. Evaluation of suspected hypothalamic disease
    3. Suspected hyperthyroidism
     
    This test is not much used nowadays due to the availability of sensitive TSH assays.
     
    Procedure
     
    • A baseline blood sample is collected for estimation of basal serum TSH level.
    • TRH is injected intravenously (200 or 500 μg) followed by measurement of serum TSH at 20 and 60 minutes.
     
    Interpretation
     
    1. Normal response: A rise of TSH > 2 mU/L at 20 minutes, and a small decline at 60 minutes.
    2. Exaggerated response: A further significant rise in already elevated TSH level at 20 minutes followed by a slight decrease at 60 minutes; occurs in primary hypothyroidism.
    3. Flat response: There is no response; occurs in secondary (pituitary) hypothyroidism.
    4. Delayed response: TSH is higher at 60 minutes as compared to its level at 20 minutes; seen in tertiary (hypothalamic) hypothyroidism.
     
    Antithyroid Antibodies
     
    Box 864.1 Thyroid autoantibodies
     
    • Useful for diagnosis and monitoring of autoimmune thyroid diseases.
    • Antimicrosomal or antithyroid peroxidase antibodies: Hashimoto’s thyroiditis
    • Anti-TSH receptor antibodies: Graves’ disease
    Various autoantibodies (TSH receptor, antimicrosomal, and antithyroglobulin) are detected in thyroid disorders like Hashimoto’s thyroiditis and Graves’ disease. Antimicrosomal (also called as thyroid peroxidase) and anti-thyroglobulin antibodies are observed in almost all patients with Hashimoto’s disease. TSH receptor antibodies (TRAb) are mainly tested in Graves’ disease to predict the outcome after treatment (Box 864.1).
     
    Radioactive Iodine Uptake (RAIU) Test
     
    This is a direct test that assesses the trapping of iodide by thyroid gland (through the iodine symporters or pumps in follicular cells) for thyroid hormone synthesis. Patient is administered a tracer dose of radioactive iodine (131I or 123I) orally. This is followed by measurement of amount of radioactivity over the thyroid gland at 2 to 6 hours and again at 24 hours. RAIU correlates directly with the functional activity of the thyroid gland. Normal RAIU is about 10-30% of administered dose at 24 hours, but varies according to the geographic location due to differences in dietary intake.
     
    Causes of Increased Uptake
     
    • Hyperthyroidism due to Graves’ disease, toxic multinodular goiter, toxic adenoma, TSH-secreting tumor.
     
    Causes of Decreased Uptake
     
    • Hyperthyroidism due to administration of thyroid hormone, factitious hyperthyroidism, subacute thyroiditis.
     
    Uses
     
    RAIU is most helpful in differential diagnosis of hyperthyroidism by separating causes into those due to increased uptake and due to decreased uptake.
     
    Thyroid Scintiscanning
     
    An isotope (99mTc-pertechnetate) is administered and a gamma counter assesses its distribution within the thyroid gland.
     
    Interpretation
     
    • Differential diagnosis of high RAIU thyrotoxicosis:
      – Graves’ disease: Uniform or diffuse increase in uptake
      – Toxic multinodular goiter: Multiple discrete areas of increased uptake
      – Adenoma: Single area of increased uptake
    • Evaluation of a solitary thyroid nodule:
      – ‘Hot’ nodule: Hyperfunctioning
      – ‘Cold’ nodule: Non-functioning; about 20% cases are malignant.
     
    Interpretation of thyroid function tests is shown in Table 164.1.
     
    Table 864.1 Interpretation of thyroid function tests
    Test results Interpretations
    1. TSH Normal, FT4 Normal Euthyroid
    2. Low TSH, Low FT4 Secondary hypothyroidism
    3. High TSH, Normal FT4 Subclinical hypothyroidism
    4. High TSH, Low FT4 Primary hypothyroidism
    5. Low TSH, Normal FT4, Normal FT3 Subclinical hyperthyroidism
    6. Low TSH, Normal FT4, High FT3 T3 toxicosis
    7. Low TSH, High FT4 Primary hyperthyroidism
     
    Neonatal Screening for Hypothyroidism
     
    Thyroid hormone deficiency during neonatal period can cause severe mental retardation (cretinism) that can be prevented by early detection and treatment. Estimation of TSH is done on dry blood spots on filter paper or cord serum between 3rd to 5th days of life. Elevated TSH is diagnostic of hypothyroidism. In infants with confirmed hypothyroidism, RAIU (123I) scan should be done to distinguish between thyroid agenesis and dyshormonogenesis.
  • DISORDERS OF THYROID
    Box 863.1 Terminology in thyroid disorders
    • Primary hyper-/hypothyroidism: Increased or decreased function of thyroid gland due to disease of thyroid itself and not due to increased or decreased levels of TRH or TSH.
    • Secondary hyper-/hypothyroidism: Increased or decreased function of thyroid gland due to increased or decreased levels of TSH.
    • Tertiary hypothyroidism: Decreased function of thyroid gland due to decreased function of hypothalamus.
    • Subclinical thyroid disease: A condition with abnormality of thyroid hormone levels in blood but without specific clinical manifestations of thyroid disease and without any history of thyroid dysfunction or therapy.
    • Subclinical hyperthyroidism: A condition with normal thyroid hormone levels but with low or undetectable TSH level.
    • Subclinical hypothyroidism: A condition with normal thyroxine and triiodothyronine level along with mildly elevated TSH level.
    Among the endocrine disorders, disorders of thyroid are common and are only next in frequency to diabetes mellitus. They are more common in women than in men. Functional thyroid disorders can be divided into two types depending on activity of the thyroid gland: hypothyroidism (low thyroid hormones), and hyperthyroidism (excess thyroid hormones). Any enlargement of thyroid gland is called as a goiter. Terminology related to thyroid disorders is shown in Box 863.1.
     
    Hyperthyroidism
     
    Hyperthyroidism is a condition caused by excessive secretion of thyroid hormone. Causes of hyperthyroidism are listed in Table 863.1.
     
    Table 863.1 Causes of hyperthyroidism
    1. Graves’ disease (Diffuse toxic goiter)
    2. Toxicity in multinodular goiter
    3. Toxicity in adenoma
    4. Subacute thyroiditis
    5. TSH-secreting pituitary adenoma (secondary hyperthyroidism)
    6. Trophoblastic tumours that secrete TSH-like hormone: choriocarcinoma, hydatidiform mole
    7. Factitious hyperthyroidism
     
    Clinical Characteristics
     
    Clinical characteristics of hyperthyroidism are nervousness, anxiety, irritability, insomnia, fine tremors; weight loss despite normal or increased appetite; heat intolerance; increased sweating; dyspnea on exertion; amenorrhea and infertility; palpitations, tachycardia, cardiac arrhythmias, heart failure (especially in elderly); and muscle weakness, proximal myopathy, and osteoporosis (especially in elderly).
     
    The triad of Graves’ disease consists of hyperthyroidism, ophthalmopathy (exophthalmos, lid retraction, lid lag, corneal ulceration, impaired eye muscle function), and dermopathy (pretibial myxoedema).
     
    Box 863.2 Thyroid function tests in hyperthyroidism
    • Thyrotoxicosis:
      Serum TSH low or undetectable
      – Raised total T4 and free T4.
    • T3 toxicosis:
      – Serum TSH undetectable
      – Normal total T4 and free T4
      – Raised T3
    Laboratory Features
     
    In most patients, free serum T3 and T4 are elevated. In T3 thyrotoxicosis (5% cases of thyrotoxicosis), serum T4 levels are normal while T3 is elevated. Serum TSH is low or undetectable (< 0.1 mU/L) (Box 863.2).
     
    Undetectable or low serum TSH along with normal levels of T3 and T4 is called as subclinical hyperthyroidism; subtle signs and symptoms of thyrotoxicosis may or may not be present. Subclinical hyperthyroidism is associated with risk of atrial fibrillation, osteoporosis, and progression to overt thyroid disease.
     
    Features of primary and secondary hyperthyroidism are compared in Table 863.2.
     
    Table 863.2 Differences between primary and secondary hyperthyroidism
    Parameter Primary hyperthyroidism Secondary hyperthyroidism
    1. Serum TSH Low Normal or high
    2. Serum free thyroxine High High
    3. TSH receptor antibodies May be positive Negative
    4. Causes Graves’ disease, toxic multinodular goiter, toxic adenoma Pituitary adenoma
     
    Evaluation of hyperthyroidism is presented in Figure 863.1.
     
    Figure 863.1 Evaluation of hyperthyroidism
    Figure 863.1 Evaluation of hyperthyroidism. TSH: thyroid stimulating hormone; FT4: free T4; FT3: free T3; TRAb: TSH receptor antibody; TRH: Thyrotropin releasing hormone
     
    Hypothyroidism
     
    Hypothyroidism is a condition caused by deficiency of thyroid hormones. Causes of hypothyroidism are listed in Table 863.3. Primary hypothyroidism results from deficient thyroid hormone biosynthesis that is not due to disorders of hypothalamus or pituitary. Secondary hypothyroidism results from deficient secretion of TSH from pituitary. Deficient or loss of secretion of thyro-tropin releasing hormone from hypothalamus results in tertiary hypothyroidism. Secondary and tertiary hypothyroidism are much less common than primary. Plasma TSH is high in primary and low in secondary and tertiary hypothyroidism. Differences between primary and secondary hypothyroidism are shown in Table 863.4.
     
    Table 863.3 Causes of hypothyroidism 
    1. Primary hypothyroidism (Increased TSH)
      • Iodine deficiency
      • Hashimoto’s thyroiditis
      Exogenous goitrogens
      • Iatrogenic: surgery, drugs, radiation
    2. Secondary hypothyroidism (Low TSH): Diseases of pituitary
    3. Tertiary hypothyroidism (Low TSH, Low TRH): Diseases of hypothalamus
     
    Table 863.4 Differences between primary and secondary hypothyroidism
    Parameter Primary hypothyroidism Secondary hypothyroidism
    1. Cause Hashimoto’s thyroiditis Pituitary disease
    2. Serum TSH High Low
    3. Thyrotropin releasing hormone stimulation test Exaggerated response No response
    4. Antimicrosomal antibodies Present Absent
     
    Box 863.3 Thyroid function tests in hypothyroidism
    • Primary hypothyroidism
      – Serum TSH: Increased (proportional to degree of hypofunction)
      – Free T4: Decreased
      – TRH stimulation test: Exaggerated response
    • Secondary hypothyroidism
      – Serum TSH: Decreased
      – Free T4: Decreased
      – TRH stimulation test: Absent response
    • Tertiary hypothyroidism
      – Serum TSH: Decreased
      – FT4: Decreased
      – TRH stimulation test: Delayed response
    Clinical features of primary hypothyroidism are: lethargy, mild depression, disturbances in menstruation, weight gain, cold intolerance, dry skin, myopathy, constipation, and firm and lobulated thyroid gland (in Hashimoto’s thyroiditis).
     
    In severe cases, myxoedema coma (an advanced stage with stupor, hypoventilation, and hypothermia) can occur.
     
    Laboratory Features
     
    Laboratory features in hypothyroidism are shown in Box 863.3.
     
    Normal serum thyroxine (T4 and FT4) coupled with a moderately raised TSH (>10 mU/L) is referred to as subclinical hypothyroidism. It is associated with bad obstetrical outcome, poor cognitive development in children, and high risk of hypercholesterolemia and progression to overt hypothyroidism.
     
    Evaluation of hypothyroidism is presented in Figure 863.2
     
    Figure 863.2 Evaluation of hypothyroidism
    Figure 863.2 Evaluation of hypothyroidism. TSH: thyroid stimulating hormone; FT4: free T4; TRH: Thyrotropin releasing hormone
  • FEMALE INFERTILITY: CAUSES AND INVESTIGATIONS
    The ovaries are the sites of production of female gametes or ova by the process of oogenesis. The ova are released by the process of ovulation in a cyclical manner at regular intervals. Ovary contains numerous follicles that contain ova in various stages of development. During each menstrual cycle, up to 20 primordial follicles are activated for maturation; however, only one follicle becomes fully mature; this dominant follicle ruptures to release the secondary oocyte from the ovary. Maturation of the follicle is stimulated by follicle stimulating hormone (FSH) secreted by anterior pituitary (Figure 862.1). Maturing follicle secretes estrogen that causes proliferation of endometrium of the uterus (proliferative phase). Follicular cells also secrete inhibin which regulates release of FSH by the anterior pituitary. Fall in FSH level is followed by secretion of luteinizing hormone (LH) by the anterior pituitary (LH surge). This causes follicle to rupture and the ovum is expelled into the peritoneal cavity near the fimbrial end of the fallopian tube. The fallopian tubes conduct ova from the ovaries to the uterus. Fertilization of ovum by the sperm occurs in the fallopian tube.
     
    Figure 862.1 The hypothalamus pituitary ovarian axis
    Figure 862.1 The hypothalamus-pituitary-ovarian axis 
     
    The ovum consists of the secondary oocyte, zona pellucida and corona radiata. The ruptured follicle in the ovary collapses and fills with blood clot (corpus luteum). LH converts granulose cells in the follicle to lutein cells which begin to secrete progesterone. Progesterone stimulates secretion from the endometrial glands (secretory phase) that were earlier under the influence of estrogen. Rising progesterone levels inhibit LH production from the anterior pituitary. Without LH, the corpus luteum regresses and becomes functionless corpus albicans. After regression of corpus luteum, production of estrogen and progesterone stops and endometrium collapses, causing onset of menstruation. If the ovum is fertilized and implanted in the uterine wall, human chorionic gonadotropin (hCG) is secreted by the developing placenta into the maternal circulation. Human chorionic gonadotropin maintains the corpus luteum for secetion of estrogen and progesterone till 12th week of pregnancy. After 12th week, corpus luteum regresses to corpus albicans and the function of synthesis of estrogen and progesterone is taken over by placenta till parturition.
     
    The average duration of the normal menstrual cycle is 28 days. Ovulation occurs around 14th day of the cycle. The time interval between ovulation and menstruation is called as luteal phase and is fairly constant (14 days) (Figure 862.2).
     
    Figure 862.2 Normal menstrual cycle
    Figure 862.2 Normal menstrual cycle
     
    Causes of Female Infertility
     
    Causes of female infertility are shown in Table 862.1.
     
    Table 862.1 Causes of female infertility
    1. Hypothalamic-pituitary dysfunction:
    • Hypothalamic causes
      – Excessive exercise
      – Excess stress
      – Low weight
      – Kallman’s syndrome
      Idiopathic
    • Pituitary causes
      – Hyperprolactinemia
      Hypopituitarism (Sheehan’s syndrome, Simmond’s disease)
      – Craniopharyngioma
      – Cerebral irradiation
     2. Ovarian dysfunction:
    • Polycystic ovarian disease (Stein-Leventhal syndrome)
    • Luteinized unruptured follicle
    • Turner’s syndrome
    • Radiation or chemotherapy
    • Surgical removal of ovaries
    • Idiopathic
     3. Dysfunction in passages:
    • Fallopian tubes
      Infections: Tuberculosis, gonorrhea, Chlamydia
      – Previous surgery (e.g. laparotomy)
      – Tubectomy
      Congenital hypoplasia, non-canalization
      Endometriosis
    • Uterus
      – Uterine malformations
      – Asherman’s syndrome
      – Tuberculous endometritis
      Fibroid
    • Cervix: Sperm antibodies
    • Vagina: Septum
     4. Dysfunction of sexual act: Dyspareunia
     
    Investigations
     
    Evaluation of female infertility is shown in Figure 862.3.
     
    Figure 862.3 Evaluation of female infertility
    Figure 862.3 Evaluation of female infertility. FSH: Follicle stimulating hormone; LH: Luteinizing hormone; DHEA-S: Dihydroepiandrosterone; TSH: Thyroid stimulating hormone; ↑ : Increased; ↓ : Decreased
     
    Tests for Ovulation
     
    Most common cause of female infertility is anovulation.
     
    1. Regular cycles, mastalgia, and laparoscopic direct visualization of corpus luteum indicate ovulatory cycles. Anovulatory cycles are clinically characterized by amenorrhea, oligomenorrhea, or irregular menstruation. However, apparently regular cycles may be associated with anovulation.
    2. Endometrial biopsy: Endometrial biopsy is done during premenstrual period (21st-23rd day of the cycle). The secretory endometrium during the later half of the cycle is an evidence of ovulation.
    3. Ultrasonography (USG): Serial ultrasonography is done from 10th day of the cycle and the size of the dominant follicle is measured. Size >18 mm is indicative of imminent ovulation. Collapse of the follicle with presence of few ml of fluid in the pouch of Douglas is suggestive of ovulation. USG also is helpful for treatment (i.e. timing of coitus or of intrauterine insemination) and diagnosis of luteinized unruptured follicle (absence of collapse of dominant follicle). Transvaginal USG is more sensitive than abdominal USG.
    4. Basal body temperature (BBT): Patient takes her oral temperature at the same time every morning before arising. BBT falls by about 0.5°F at the time of ovulation. During the second (progestational) half of the cycle, temperature is slightly raised above the preovulatory level (rise of 0.5° to 1°F). This is due to the slight pyrogenic action of progesterone and is therefore presumptive evidence of functional corpus luteum.
    5. Cervical mucus study:
      Fern test: During estrogenic phase, a characteristic pattern of fern formation is seen when cervical mucus is spread on a glass slide (Figure 862.4). This ferning disappears after the 21st day of the cycle. If previously observed, its disappearance is presumptive evidence of corpus luteum activity.
      Spinnbarkeit test: Cervical mucus is elastic and withstands stretching upto a distance of over 10 cm. This phenomenon is called Spinnbarkeit or the thread test for the estrogen activity. During the secretory phase, viscosity of the cervical mucus increases and it gets fractured when stretched. This change in cervical mucus is evidence of ovulation.
    6. Vaginal cytology: Karyopyknotic index (KI) is high during estrogenic phase, while it becomes low in secretory phase. This refers to percentage of super-ficial squamous cells with pyknotic nuclei to all mature squamous cells in a lateral vaginal wall smear. Usually minimum of 300 cells are evaluated. The peak KI usually corresponds with time of ovulation and may reach upto 50 to 85.
    7. Estimation of progesterone in mid-luteal phase (day 21 or 7 days before expected menstruation): Progesterone level > 10 nmol/L is a reliable evidence of ovulation if cycles are regular (Figure 862.5). A mistimed sample is a common cause of abnormal result.
     
    Figure 862.4 Ferning of cervical mucosa
    Figure 862.4 Ferning of cervical mucosa
     
    Figure 862.5 Serum progesterone during normal menstrual cycle
    Figure 862.5 Serum progesterone during normal menstrual cycle
     
    Tests to Determine the Cause of Anovulation
     
    1. Measurement of LH, FSH, and estradiol during days 2 to 6: All values are low in hypogonadotropic hypogonadism (hypothalamic or pituitary failure).
    2. Measurement of TSH, prolactin, and testosterone if cycles are irregular or absent:
      Increased TSH: Hypothyroidism
      Increased prolactin: Pituitary adenoma
      Increased testosterone: Polycystic ovarian disease (PCOD), congenital adrenal hyperplasia (To differentiate PCOD from congenital adrenal hyperplasia, ultrasound and estimation of dihydroepiandrosterone or DHEA are done).
    3. Transvaginal ultrasonography: This is done for detection of PCOD.
     
    Investigations to Assess Tubal and Uterine Status
     
    1. Infectious disease: These tests include endometrial biopsy for tuberculosis and test for chlamydial IgG antibodies for tubal factor in infertility.
    2. Hysterosalpingography (HSG): HSG is a radiological contrast study for investigation of the shape of the uterine cavity and for blockage of fallopian tubes (Figure 862.6). A catheter is introduced into the cervical canal and a radiocontrast dye is injected into the uterine cavity. A real time X-ray imaging is carried out to observe the flow of the dye into the uterine cavity, tubes, and spillage into the uterine cavity.
    3. Hysterosalpingo-contrast sonography: A catheter is introduced into the cervical canal and an echocontrast fluid is introduced into the uterine cavity. Shape of the uterine cavity, filling of fallopian tubes, and spillage of contrast fluid are noted. In addition, ultrasound scan of the pelvis provides information about any fibroids or polycystic ovarian disease.
    4. Laparoscopy and dye hydrotubation test with hysteroscopy: In this test, a cannula is inserted into the cervix and methylene blue dye is introduced into the uterine cavity. If tubes are patent, spillage of the dye is observed from the ends of both tubes. This technique also allows visualization of pelvic organs, endometriosis, and pelvic adhesions. If required, endometriosis and tubal blockage can be treated during the procedure.
     
    Possible pregnancy and active pelvic or vaginal infection are contraindications to tubal patency tests.
     
    Figure 862.6 Hysterosalpingography
    Figure 862.6 Hysterosalpingography
Advertisement

Useful Sites

  • NCBI

    National Center for Biotechnology Information
  • LTO

    Lab Tests Online® by AACC
  • ASCP

    American Society for Clinical Pathology
  • ASM

    American Society for Microbiology
  • The Medical Library®

    Project of BioScience.pk
Advertisement

Connect With Us

Contact Us

All comments and suggestions about this web site are very welcome and a valuable source of information for us. Thanks!

Tel: +(92) 302 970 8985-6

Email: This email address is being protected from spambots. You need JavaScript enabled to view it.

Website: https://www.bioscience.pk



This website is certified by Health On the Net Foundation. Click to verify. This site complies with the HONcode standard for trustworthy health information:
verify here.

Our Sponsors

InsightGadgets.comPathLabStudyTheMedicalLibrary.orgThe Physio ClubB2BPakistan.com

By using BioScience.pk you agree to our use of cookies to enhance your experience on this website.