PCL
Investigation
• It is a diagnosis of exclusion
• Rome III [2006]criteria
o Recurrent abdominal pain or discomfort at least 3 days/month in the last 3 months associated with two or more of the following:
Improvement with defecation
Onset associated with changes in frequency of stool
Onset associated with changes in form (appearance) of stool
o Criterion fulfilled for the last 3 months with symptoms onset at least 6 months prior diagnosis
• Manning’s Criteria
o Onset of pain linked to more frequent bowel movements
o Looser stools associated with onset of pain
o Pain relieved by passage of stool
o Noticeable abdominal bloating
o Sensation of incomplete evacuation more than 25% of the time
o Diarrhea with mucus more than 25% of the time
• Full blood count, X-ray, Colonoscopy, Gastroscopy, Sigmoidoscopy, CT, MRI. Important to note patients’ age and risk factors for differential diagnosis.
• Infectious diseases, Coeliac disease, Helicobacter pylori and Inflammatory bowel diesease
Treatment Options
• Diet
o Lactose intolerance – lactose free diet
o Fructose malabsoption – Restrict fructose and fructan intake
o Over eating or drinking may provoke gastrocolic response due to heightened sensitivity.
o Fibre – soluble fibre [psyllium] is found to be effective in the general IBS population especially to those who have constipation that is predominant of irritable bowel. However, it doesn’t reduce pain.
• Medication
o Antispasmodic [anticholinergic - hysocyamine or dicyclomine]
Patients with cramps or diarrhea
o Stool softener or Laxatives
Osmotic [Polyethylene glycol]
Stimulant - Cathartic colon
Lubiprostone is also a drug that helps chronic idiopathic constipation
o Antidiarrheals
Opiate or Opioid analogs such as loperamide and diphenoxylate
o Serotonin - Improves gut motility
Agonist [Tegaserod, SSRI] improves constipation predominant pain/diarrhea
Antagonist [Alosetron] improves pain/diarrhea predominant constipation
o Tricyclic antidepressants
Low dose can be effective
o Antibiotic
Rifaximin can be used for bloating and flatulence, suggesting bacterial overgrowth
• Psychotherapy
o Brain-gut
o Cognitive behavioural therapy and hypnosis
• Alternative medicine
o Probiotics - Yogurt
o Yoga
o Herbal remedies
o Accupuncture
we come in many different colors and flavors (:
Showing posts with label Treatment. Show all posts
Showing posts with label Treatment. Show all posts
Wednesday, August 11, 2010
Tuesday, August 10, 2010
Investigations, Treatment and the Infamous Gluten Free Diet
Investigations for Coeliac disease
Because CD is considerably under-diagnosed in Primary Care,consider the diagnosis and perform serological testing in all patients who present with:
•chronic or intermittent diarrhoea
•failure to thrive or faltering growth in children
•persistent or unexplained gastrointestinal symptoms including nausea and vomiting
•prolonged fatigue ('tired all the time')
•recurrent abdominal pain, cramping or distension
•sudden or unexpected weight loss
•unexplained iron-deficiency anaemia, or other unspecified anaemia
Serology – make sure they have been on a gluten diet for at least 6 weeks
•IgA anti-tissue transglutaminase antibodies (tTGAs) is the preferred investigation. Endomysial antibodies (EMAs) are used if tTGA) test is not available or equivocal.
•False negatives occur if the patient has selective IgA deficiency, as occurs in ~0.4% of the general population14 and in 2.6% of patients with CD (laboratories should test for IgA deficiency on negative samples). Use IgG tTGA and/or IgG EMA serological tests for people with confirmed IgA deficiency.
•Antibodies frequently become undetectable after 6-12 months of a GFD and thus can be used to monitor the disease.
Antigliadin antibodies are no longer recommended - they are less specific, but can be either IgA (AGA) or IgG (AGG). They can be positive in other gastrointestinal conditions such as Crohn's disease
Biopsy
Patients with positive serological tests should be offered referral to local gastroenterologist for endoscopic or enteroscopic distal duodenal or jejunal biopsy to confirm diagnosis. They need to stay on gluten until after the biopsy. Referral should also be made where the serology is negative but there is still clinical suspicion of CD.
•The diagnosis of CD is made when biopsy shows villous atrophy while the patient is eating adequate amounts of gluten, followed by full clinical remission on excluding gluten.
•Under these circumstances, tTGA or EMA antibodies found at the time of diagnosis and their disappearance after gluten exclusion, means that it is only necessary to perform a further biopsy (and even a further gluten challenge and more biopsies) if there are still doubts. The further gluten challenge should always be performed if CD is diagnosed in children less than 2 yrs because of a high incidence of other causes of flat mucosa.
Other investigations
•FBC shows anaemia in 50%; iron and folate deficiency are both common (microcytes and macrocytes), hypersegmented leucocytes and Howell-Jolly bodies (splenic atrophy). Also check B12, folate, ferritin, LFT, calcium and albumin.
•Small bowel barium studies are occasionally needed to exclude other causes of malabsorption and diarrhoea, and diagnose rare complications such as obstruction or lymphoma.
Treatment
Starting a GFD rapidly induces clinical improvement, which is mirrored by the mucosa. The diet consists of no wheat, barley, rye, or any food containing them (e.g. bread, cake, pies). Moderate quantities of oats (free from other contaminating cereals) can be consumed as recent studies suggest that they do not damage the intestinal mucosa. Rice, maize, soya, potatoes, sugar jam, syrup and treacle are all allowed. Gluten-free biscuits, flour, bread and pasta are NHS prescribable. Coeliac UK produces a prescribing guide. When making GFD, must make sure cross contamination doesn’t occur, as a person with celiac can only take 0.02% of gluten in a product safely and even a little cross contamination with wheat (12% gluten) may result in return of symptoms.
Arrange dietitian appointment (with regular reviews). Even minor dietary lapses may cause recurrence. GFD should be lifelong, as relaxation of diet generally brings a return of symptoms and increased incidence of complications. Add supplements as necessary (e.g. folic acid, iron, calcium and vitamin D).
Serial tTGA or EMA antibodies can be used to monitor response to diet.
Oats - there was originally some concern about including oats in a GFD, but recent research has emphasised that oats can be given to almost all patients with coeliac disease.
Oral proteases are being developed (which digest gluten) and these may offer therapeutic options in the future.
Why follow up patients with coeliac disease?
Patient compliance with a GFD is poor, ranging from 45-87%. The long-term health risks for patients who comply poorly with a GFD include nutritional deficiency and reduced bone mineral density.
About a quarter of patients with CD have osteoporosis of the lumbar spine compared to 5% of matched controls. Bone mineral density improves significantly with a GFD.
Dietary compliance positively correlates with regular follow-up and knowledge of the condition.
Half of all coeliac patients have an inadequate energy intake, and 10% have inadequate intake of calcium and vitamin B6. 80% of elderly patients have inadequate intake of vitamin D.
GPs are responsible for the appropriate prescription of gluten-free products.20
Regular follow-up is an opportunity to provide patient-centred care that is sensitive to the individual's life circumstances.
How often should patients be reviewed?
Patients should be followed up throughout their lifetime.
After diagnosis, the patient should be reviewed at the gastroenterology clinic after 3 months and 6 months to ensure they are making satisfactory progress and managing the diet.
If well, they should be reviewed annually or sooner if problems arise - follow-up assessments are currently being carried out by dietitians, nurses, general practitioners and gastroenterologists in primary and secondary care.
GFD
- Jewish holiday Passover contains mostly gluten free food (except Maztah); usually stocked in early spring in stores catering to Jews.
Obvious Gluten
Less Obvious Gluten
High in Vitamin D
Iron Rich food
Naturally Gluten Free
Because CD is considerably under-diagnosed in Primary Care,consider the diagnosis and perform serological testing in all patients who present with:
•chronic or intermittent diarrhoea
•failure to thrive or faltering growth in children
•persistent or unexplained gastrointestinal symptoms including nausea and vomiting
•prolonged fatigue ('tired all the time')
•recurrent abdominal pain, cramping or distension
•sudden or unexpected weight loss
•unexplained iron-deficiency anaemia, or other unspecified anaemia
Serology – make sure they have been on a gluten diet for at least 6 weeks
•IgA anti-tissue transglutaminase antibodies (tTGAs) is the preferred investigation. Endomysial antibodies (EMAs) are used if tTGA) test is not available or equivocal.
•False negatives occur if the patient has selective IgA deficiency, as occurs in ~0.4% of the general population14 and in 2.6% of patients with CD (laboratories should test for IgA deficiency on negative samples). Use IgG tTGA and/or IgG EMA serological tests for people with confirmed IgA deficiency.
•Antibodies frequently become undetectable after 6-12 months of a GFD and thus can be used to monitor the disease.
Antigliadin antibodies are no longer recommended - they are less specific, but can be either IgA (AGA) or IgG (AGG). They can be positive in other gastrointestinal conditions such as Crohn's disease
Biopsy
Patients with positive serological tests should be offered referral to local gastroenterologist for endoscopic or enteroscopic distal duodenal or jejunal biopsy to confirm diagnosis. They need to stay on gluten until after the biopsy. Referral should also be made where the serology is negative but there is still clinical suspicion of CD.
•The diagnosis of CD is made when biopsy shows villous atrophy while the patient is eating adequate amounts of gluten, followed by full clinical remission on excluding gluten.
•Under these circumstances, tTGA or EMA antibodies found at the time of diagnosis and their disappearance after gluten exclusion, means that it is only necessary to perform a further biopsy (and even a further gluten challenge and more biopsies) if there are still doubts. The further gluten challenge should always be performed if CD is diagnosed in children less than 2 yrs because of a high incidence of other causes of flat mucosa.
Other investigations
•FBC shows anaemia in 50%; iron and folate deficiency are both common (microcytes and macrocytes), hypersegmented leucocytes and Howell-Jolly bodies (splenic atrophy). Also check B12, folate, ferritin, LFT, calcium and albumin.
•Small bowel barium studies are occasionally needed to exclude other causes of malabsorption and diarrhoea, and diagnose rare complications such as obstruction or lymphoma.
Treatment
Starting a GFD rapidly induces clinical improvement, which is mirrored by the mucosa. The diet consists of no wheat, barley, rye, or any food containing them (e.g. bread, cake, pies). Moderate quantities of oats (free from other contaminating cereals) can be consumed as recent studies suggest that they do not damage the intestinal mucosa. Rice, maize, soya, potatoes, sugar jam, syrup and treacle are all allowed. Gluten-free biscuits, flour, bread and pasta are NHS prescribable. Coeliac UK produces a prescribing guide. When making GFD, must make sure cross contamination doesn’t occur, as a person with celiac can only take 0.02% of gluten in a product safely and even a little cross contamination with wheat (12% gluten) may result in return of symptoms.
Arrange dietitian appointment (with regular reviews). Even minor dietary lapses may cause recurrence. GFD should be lifelong, as relaxation of diet generally brings a return of symptoms and increased incidence of complications. Add supplements as necessary (e.g. folic acid, iron, calcium and vitamin D).
Serial tTGA or EMA antibodies can be used to monitor response to diet.
Oats - there was originally some concern about including oats in a GFD, but recent research has emphasised that oats can be given to almost all patients with coeliac disease.
Oral proteases are being developed (which digest gluten) and these may offer therapeutic options in the future.
Why follow up patients with coeliac disease?
Patient compliance with a GFD is poor, ranging from 45-87%. The long-term health risks for patients who comply poorly with a GFD include nutritional deficiency and reduced bone mineral density.
About a quarter of patients with CD have osteoporosis of the lumbar spine compared to 5% of matched controls. Bone mineral density improves significantly with a GFD.
Dietary compliance positively correlates with regular follow-up and knowledge of the condition.
Half of all coeliac patients have an inadequate energy intake, and 10% have inadequate intake of calcium and vitamin B6. 80% of elderly patients have inadequate intake of vitamin D.
GPs are responsible for the appropriate prescription of gluten-free products.20
Regular follow-up is an opportunity to provide patient-centred care that is sensitive to the individual's life circumstances.
How often should patients be reviewed?
Patients should be followed up throughout their lifetime.
After diagnosis, the patient should be reviewed at the gastroenterology clinic after 3 months and 6 months to ensure they are making satisfactory progress and managing the diet.
If well, they should be reviewed annually or sooner if problems arise - follow-up assessments are currently being carried out by dietitians, nurses, general practitioners and gastroenterologists in primary and secondary care.
GFD
- Jewish holiday Passover contains mostly gluten free food (except Maztah); usually stocked in early spring in stores catering to Jews.
Obvious Gluten
Less Obvious Gluten
High in Vitamin D
Iron Rich food
Naturally Gluten Free
Wednesday, May 19, 2010
Treatment of Nephrotic Syndrome
Treatments of Nephrotic Syndrome
Treat the complications
Peripheral Edema
• frusemide, spironolactone as diuretics
• CIx – albumin serum level <1.5 g/dL (N-3.4 - 5.4 g/dL)
Protein Loss (Proteinuria)
• dietary protein intake should replace the daily urinary protein losses
• protein restriction to 0.6 - 0.8 g/kg/d shows mild benefit but great care must be taken so there is no malnutrition.
• ACE inhibitors or ARB. (Lisinopril | Losartan [for those unable tolerate ACE I - cough] )
o Reducing blood pressure by reducing intraglomerular pressure and direct action of podocytes (increasing their population)
Hyperlipidemia
• statin (Lovastatin)
• hyperlidpidemia always be there unless nephrotic syndrome is treated
Hypercoagulable State
• serum albumin < 2 g/dL can become hypercoagulable.
• taken by ppl prone to renal vein thrombosis and other tromboemboli but not as primary prevention.
Treat underlying cause
• Systemic Lupus Erythematosus [causes lupus nephritis, autoimmune disease]
o Immunomodulators
Cyclophosphamide [prodrug - liver]
Useful for relapse steroid sensitive nephrotic syndrome
• Minimal Change Nephropathy [histopathologic lesion in the glomerulus]
o Corticosteroids
Prenidisone [prodrug - liver]
• Amyloidosis [extracellular tissue deposition of fibrils composed of fragments of serum amyloid A (SAA) protein.]
Treat the complications
Peripheral Edema
• frusemide, spironolactone as diuretics
• CIx – albumin serum level <1.5 g/dL (N-3.4 - 5.4 g/dL)
Protein Loss (Proteinuria)
• dietary protein intake should replace the daily urinary protein losses
• protein restriction to 0.6 - 0.8 g/kg/d shows mild benefit but great care must be taken so there is no malnutrition.
• ACE inhibitors or ARB. (Lisinopril | Losartan [for those unable tolerate ACE I - cough] )
o Reducing blood pressure by reducing intraglomerular pressure and direct action of podocytes (increasing their population)
Hyperlipidemia
• statin (Lovastatin)
• hyperlidpidemia always be there unless nephrotic syndrome is treated
Hypercoagulable State
• serum albumin < 2 g/dL can become hypercoagulable.
• taken by ppl prone to renal vein thrombosis and other tromboemboli but not as primary prevention.
Treat underlying cause
• Systemic Lupus Erythematosus [causes lupus nephritis, autoimmune disease]
o Immunomodulators
Cyclophosphamide [prodrug - liver]
Useful for relapse steroid sensitive nephrotic syndrome
• Minimal Change Nephropathy [histopathologic lesion in the glomerulus]
o Corticosteroids
Prenidisone [prodrug - liver]
• Amyloidosis [extracellular tissue deposition of fibrils composed of fragments of serum amyloid A (SAA) protein.]
Wednesday, April 21, 2010
Investigations and Treatment for Hyponatremia
Investigations
• The diagnosis of hyponatremia: Concentration of sodium in serum
• There may be errors for eg, if sample obtained from site just proximal to infusion of hypotonic saline/ dextrose in water
• Hyperglycemia may lead to low serum sodium levels but it isn’t a true hyposmolar state, as hyperglycemia causes a shift of free water from intracellular to extracellular space thereby diluting the sodium (by a factor of 1.6 mEq/L for each 100 mg/dL increase above normal serum glucose concentration). Concentration resumed once normoglycemia re-established.
• Hyponatremia may be noted in patients whose serum contains unusually large quantities of protein or lipid.
o In these patients, an expanded plasma protein or lipid fraction leads to a decrease in the plasma water fraction in which sodium is dissolved.
o Laboratory techniques that measure absolute sodium content per unit of plasma water report low sodium levels despite the fact that the concentration of sodium in serum water remains within the normal range.
o This phenomenon is known as pseudohyponatremia,
o Hyperlipidemia that is severe enough to produce pseudohyponatremia almost always is accompanied by a notably lipemic appearance of the serum sample.
o Hyperproteinemia of sufficient magnitude to induce pseudohyponatremia commonly is due to coexisting multiple myeloma.
Serum osmolarity: Helpful in establishing the diagnosis of true hyposmolar hyponatremia. Serum osmolarity is abnormally low in patients with hyposmolar hyponatremia, but it is normal in patients with pseudohyponatremia due to hyperlipidemia or hyperproteinemia and normal or elevated in patients with hypertonic hyponatremia due to serum hyperglycemia.
Urine sodium levels
• Hypovolemic hyponatremia: Non-renal: Vomiting, diarrhea, fistulas, GI drainage and third spacing of fluids have avid renal absorption of tubular sodium and urine sodium levels of less than 20 mEq/L. Renal: Diuretics, salt-losing nephropathy and aldosterone deficiency have elevated urine sodium levels in excess of 20 mEq/L.
• Hypervolemic hyponatremia: Non-renal: decrease in circulating volume (eg, cirrhosis, nephrosis, congestive heart failure) have urine sodium levels of less than 20 mEq/L. Renal: (SIADH) have urine sodium levels in excess of 20 mEq/L.
Urine osmolarity may be helpful in establishing the diagnosis of SIADH. Typically, patients with SIADH have inappropriately concentrated urine, with urine osmolarities in excess of 100 mOsm/L. Other forms of hyponatremia doesn’t result in such concentrated urine (normal ADH levels)
Serum thyroid-stimulating hormone (TSH) and free thyroxin levels should be checked if the clinical presentation is consistent with hypothyroidism.
Adrenal function should be assessed, via random serum cortisol levels or adrenocorticotropic hormone (ACTH) stimulation test, in patients who have recently taken oral steroids or in any patient suspected of having cortisol deficiency.
Serum ADH levels are not routinely used in the evaluation of hyponatremia because the assay is technically difficult and not widely available on a stat basis. Recently, a serum peptide known as copeptin has been studied in the evaluation of hyponatremia. Copeptin is the C terminal portion of provasopressin and is released in equimolar amounts with vasopressin (ADH).
Imaging Studies: A head CT scan is indicated in patients with altered mental status to ensure that no other underlying cause for the mental status is present.
Treatments
Emergency Care
• Supply O2 and IV glucose in hypoglycaemic patients who exhibit lethargy.
• Anticonvulsant therapy to patients experiencing seizures but if it is secondary to hyponatremia, unlikely to respond but still should do it until diagnosis is made.
• Intubate and initiate hyperventilation to reduce intracranial pressure in patients exhibiting signs of brainstem herniation (eg: fixed, unilateral, dilated pupil; decorticate posturing) until a more definitive therapy can be initiated.
• Avoid giving hypotonic intravenous fluids because they may exacerbate cerebral edema.
Acute hyponatremia (less common)
• Typically is seen in patients with a history of sudden free water loading (eg, patients with psychogenic polydipsia, infants fed tap water for 1-2 d, patients given hypotonic fluids in the postoperative period).
• Acute evolution of hyponatremia leaves little opportunity for compensatory extrusion of CNS intracellular solutes.
• The ultimate danger for these patients is brainstem herniation when sodium levels fall below 120 mEq/L.
• The therapeutic goal is to increase the serum sodium level rapidly by 4-6 mEq/L over the first 1-2 hours.
• The source of free water must be identified and eliminated.
• In patients with healthy renal function and mild to moderately severe symptoms, the serum sodium level may correct spontaneously without further intervention.
• Patients with seizures, severe confusion, coma, or signs of brainstem herniation should receive hypertonic (3%) saline to rapidly correct serum sodium level toward normal but only enough to arrest the progression of symptoms. An increase in serum sodium level of 4-6 mEq/L is generally sufficient. Any further correction is potentially dangerous and must be avoided unless necessary to correct continued seizures or other severe CNS abnormality.
Chronic hyponatremia (more common)
• Patients with mild symptoms and a serum sodium level of 125 mEq/L or less often have chronic hyponatremia. These patients lack any history of sudden free water loading.
• Chronic hyponatremia must be managed with extreme care; treatment of chronic hyponatremia has been associated with the development of the osmotic demyelination syndrome characterized by focal demyelination in the pons and extrapontine areas associated with serious neurologic sequelae.
• Management should include meticulous attention to adequate oxygenation and a gradual increase in serum sodium level to 120-125 mEq/L. Serum sodium level should not be allowed to reach normal levels or hypernatremic levels within the first 48 hours.
• The risk of osmotic demyelination appears to be minimal in patients whose chronic hyponatremia is corrected at a rate not to exceed 10-12 mEq/L in the first 24 hours and not to exceed 18 mEq/L in the first 48 hours
• Patients with chronic hyponatremia and severe symptoms (eg, severe confusion, coma, seizures) should receive hypertonic saline but only enough to raise the serum sodium level by 4-6 mEq/L and to arrest seizure activity.
o Further correction should proceed at an overall rate that is no greater than 10-12 mEq/L in the first 24 hours and no greater than 18 mEq/L in the first 48 hours.
• In treating patients with chronic hyponatremia and mild to moderately severe symptoms, consider the cause of the hyponatremic state. Patients are classified as having hypovolemic, euvolemic, or hypervolemic hyponatremia based on historical clues and physical examination. Regardless of the therapeutic approach, serum sodium must be monitored closely and corrected no faster than 10-12 mEq/L in the first 24 hours and 18 mEq/L in the first 48 hours.
o Hypovolemic hyponatremia: Patients have decreased total body sodium stores. If symptoms are mild to moderately severe, treat with isotonic saline; monitor serum sodium levels frequently to ensure that the serum sodium level increases slowly.
o Hypervolemic hyponatremia: Patients have increased total body sodium stores. Treatment consists of sodium and water restriction and attention to the underlying cause. The vasopressin receptor antagonists conivaptan (Vaprisol) and tolvaptan (Samsca) are used in hospitalized patients with hypervolemic hyponatremia.
o Euvolemic hyponatremia: This implies normal sodium stores and a total body excess of free water. Treatment consists of free water restriction and correction of the underlying condition. Recently developed AVP (vasopressin) receptor antagonists (eg, conivaptan, tolvaptan) show promise as effective and well-tolerated intravenous therapy for SIADH. Further studies are needed to better define their role in the treatment of hyponatremia associated with SIADH
Hypertonic Saline
Sodium Requirement (mEq) = TBW (Desired Na - Serum Na) where TBW = Body Weight X 0.6
Volume of Hypertonic Saline = Na Requirement (mEq) X 1000 / Infusate Na Concentration (mEq/L)
For example, a 60-kg woman with serum sodium level of 113 mEq/L would require 280 mL of hypertonic saline in order to increase serum sodium by 4 mEq/L (could be administered as 140 mL/h for 2 h)
In general, 200-400 mL of 3% NaCl is reasonable dose in most adult patients with severe symptomatic hyponatremia
Give IV over first 1-2 h until resolution of seizures or herniation
Arginine vasopressin antagonists (Conivaptan: non-selective, Tolvaptam: selective)
These agents treat hyponatremia through V2 antagonism of AVP in the renal collecting ducts. This effect results in aquaresis (excretion of free water).
Arginine vasopressin antagonist Conivaptan (V1A, V2) indicated for euvolemic and hypervolemic hyponatremia. Increases urine output of mostly free water, with little electrolyte loss.
Selective vasopressin V2 -receptor antagonist Tolvaptam, indicated for hypervolemic and euvolemic hyponatremia (i.e., serum sodium level <125 mEq/L) or less marked hyponatremia that is symptomatic and has resisted correction with fluid restriction. Used for hyponatremia associated with congestive heart failure, liver cirrhosis, and syndrome of inappropriate antidiuretic hormone secretion. Initiate or reinitiate in hospital environment only.
http://emedicine.medscape.com/article/767624-treatment
• The diagnosis of hyponatremia: Concentration of sodium in serum
• There may be errors for eg, if sample obtained from site just proximal to infusion of hypotonic saline/ dextrose in water
• Hyperglycemia may lead to low serum sodium levels but it isn’t a true hyposmolar state, as hyperglycemia causes a shift of free water from intracellular to extracellular space thereby diluting the sodium (by a factor of 1.6 mEq/L for each 100 mg/dL increase above normal serum glucose concentration). Concentration resumed once normoglycemia re-established.
• Hyponatremia may be noted in patients whose serum contains unusually large quantities of protein or lipid.
o In these patients, an expanded plasma protein or lipid fraction leads to a decrease in the plasma water fraction in which sodium is dissolved.
o Laboratory techniques that measure absolute sodium content per unit of plasma water report low sodium levels despite the fact that the concentration of sodium in serum water remains within the normal range.
o This phenomenon is known as pseudohyponatremia,
o Hyperlipidemia that is severe enough to produce pseudohyponatremia almost always is accompanied by a notably lipemic appearance of the serum sample.
o Hyperproteinemia of sufficient magnitude to induce pseudohyponatremia commonly is due to coexisting multiple myeloma.
Serum osmolarity: Helpful in establishing the diagnosis of true hyposmolar hyponatremia. Serum osmolarity is abnormally low in patients with hyposmolar hyponatremia, but it is normal in patients with pseudohyponatremia due to hyperlipidemia or hyperproteinemia and normal or elevated in patients with hypertonic hyponatremia due to serum hyperglycemia.
Urine sodium levels
• Hypovolemic hyponatremia: Non-renal: Vomiting, diarrhea, fistulas, GI drainage and third spacing of fluids have avid renal absorption of tubular sodium and urine sodium levels of less than 20 mEq/L. Renal: Diuretics, salt-losing nephropathy and aldosterone deficiency have elevated urine sodium levels in excess of 20 mEq/L.
• Hypervolemic hyponatremia: Non-renal: decrease in circulating volume (eg, cirrhosis, nephrosis, congestive heart failure) have urine sodium levels of less than 20 mEq/L. Renal: (SIADH) have urine sodium levels in excess of 20 mEq/L.
Urine osmolarity may be helpful in establishing the diagnosis of SIADH. Typically, patients with SIADH have inappropriately concentrated urine, with urine osmolarities in excess of 100 mOsm/L. Other forms of hyponatremia doesn’t result in such concentrated urine (normal ADH levels)
Serum thyroid-stimulating hormone (TSH) and free thyroxin levels should be checked if the clinical presentation is consistent with hypothyroidism.
Adrenal function should be assessed, via random serum cortisol levels or adrenocorticotropic hormone (ACTH) stimulation test, in patients who have recently taken oral steroids or in any patient suspected of having cortisol deficiency.
Serum ADH levels are not routinely used in the evaluation of hyponatremia because the assay is technically difficult and not widely available on a stat basis. Recently, a serum peptide known as copeptin has been studied in the evaluation of hyponatremia. Copeptin is the C terminal portion of provasopressin and is released in equimolar amounts with vasopressin (ADH).
Imaging Studies: A head CT scan is indicated in patients with altered mental status to ensure that no other underlying cause for the mental status is present.
Treatments
Emergency Care
• Supply O2 and IV glucose in hypoglycaemic patients who exhibit lethargy.
• Anticonvulsant therapy to patients experiencing seizures but if it is secondary to hyponatremia, unlikely to respond but still should do it until diagnosis is made.
• Intubate and initiate hyperventilation to reduce intracranial pressure in patients exhibiting signs of brainstem herniation (eg: fixed, unilateral, dilated pupil; decorticate posturing) until a more definitive therapy can be initiated.
• Avoid giving hypotonic intravenous fluids because they may exacerbate cerebral edema.
Acute hyponatremia (less common)
• Typically is seen in patients with a history of sudden free water loading (eg, patients with psychogenic polydipsia, infants fed tap water for 1-2 d, patients given hypotonic fluids in the postoperative period).
• Acute evolution of hyponatremia leaves little opportunity for compensatory extrusion of CNS intracellular solutes.
• The ultimate danger for these patients is brainstem herniation when sodium levels fall below 120 mEq/L.
• The therapeutic goal is to increase the serum sodium level rapidly by 4-6 mEq/L over the first 1-2 hours.
• The source of free water must be identified and eliminated.
• In patients with healthy renal function and mild to moderately severe symptoms, the serum sodium level may correct spontaneously without further intervention.
• Patients with seizures, severe confusion, coma, or signs of brainstem herniation should receive hypertonic (3%) saline to rapidly correct serum sodium level toward normal but only enough to arrest the progression of symptoms. An increase in serum sodium level of 4-6 mEq/L is generally sufficient. Any further correction is potentially dangerous and must be avoided unless necessary to correct continued seizures or other severe CNS abnormality.
Chronic hyponatremia (more common)
• Patients with mild symptoms and a serum sodium level of 125 mEq/L or less often have chronic hyponatremia. These patients lack any history of sudden free water loading.
• Chronic hyponatremia must be managed with extreme care; treatment of chronic hyponatremia has been associated with the development of the osmotic demyelination syndrome characterized by focal demyelination in the pons and extrapontine areas associated with serious neurologic sequelae.
• Management should include meticulous attention to adequate oxygenation and a gradual increase in serum sodium level to 120-125 mEq/L. Serum sodium level should not be allowed to reach normal levels or hypernatremic levels within the first 48 hours.
• The risk of osmotic demyelination appears to be minimal in patients whose chronic hyponatremia is corrected at a rate not to exceed 10-12 mEq/L in the first 24 hours and not to exceed 18 mEq/L in the first 48 hours
• Patients with chronic hyponatremia and severe symptoms (eg, severe confusion, coma, seizures) should receive hypertonic saline but only enough to raise the serum sodium level by 4-6 mEq/L and to arrest seizure activity.
o Further correction should proceed at an overall rate that is no greater than 10-12 mEq/L in the first 24 hours and no greater than 18 mEq/L in the first 48 hours.
• In treating patients with chronic hyponatremia and mild to moderately severe symptoms, consider the cause of the hyponatremic state. Patients are classified as having hypovolemic, euvolemic, or hypervolemic hyponatremia based on historical clues and physical examination. Regardless of the therapeutic approach, serum sodium must be monitored closely and corrected no faster than 10-12 mEq/L in the first 24 hours and 18 mEq/L in the first 48 hours.
o Hypovolemic hyponatremia: Patients have decreased total body sodium stores. If symptoms are mild to moderately severe, treat with isotonic saline; monitor serum sodium levels frequently to ensure that the serum sodium level increases slowly.
o Hypervolemic hyponatremia: Patients have increased total body sodium stores. Treatment consists of sodium and water restriction and attention to the underlying cause. The vasopressin receptor antagonists conivaptan (Vaprisol) and tolvaptan (Samsca) are used in hospitalized patients with hypervolemic hyponatremia.
o Euvolemic hyponatremia: This implies normal sodium stores and a total body excess of free water. Treatment consists of free water restriction and correction of the underlying condition. Recently developed AVP (vasopressin) receptor antagonists (eg, conivaptan, tolvaptan) show promise as effective and well-tolerated intravenous therapy for SIADH. Further studies are needed to better define their role in the treatment of hyponatremia associated with SIADH
Hypertonic Saline
Sodium Requirement (mEq) = TBW (Desired Na - Serum Na) where TBW = Body Weight X 0.6
Volume of Hypertonic Saline = Na Requirement (mEq) X 1000 / Infusate Na Concentration (mEq/L)
For example, a 60-kg woman with serum sodium level of 113 mEq/L would require 280 mL of hypertonic saline in order to increase serum sodium by 4 mEq/L (could be administered as 140 mL/h for 2 h)
In general, 200-400 mL of 3% NaCl is reasonable dose in most adult patients with severe symptomatic hyponatremia
Give IV over first 1-2 h until resolution of seizures or herniation
Arginine vasopressin antagonists (Conivaptan: non-selective, Tolvaptam: selective)
These agents treat hyponatremia through V2 antagonism of AVP in the renal collecting ducts. This effect results in aquaresis (excretion of free water).
Arginine vasopressin antagonist Conivaptan (V1A, V2) indicated for euvolemic and hypervolemic hyponatremia. Increases urine output of mostly free water, with little electrolyte loss.
Selective vasopressin V2 -receptor antagonist Tolvaptam, indicated for hypervolemic and euvolemic hyponatremia (i.e., serum sodium level <125 mEq/L) or less marked hyponatremia that is symptomatic and has resisted correction with fluid restriction. Used for hyponatremia associated with congestive heart failure, liver cirrhosis, and syndrome of inappropriate antidiuretic hormone secretion. Initiate or reinitiate in hospital environment only.
http://emedicine.medscape.com/article/767624-treatment
Sunday, March 28, 2010
Treatment of Sleep Apnea
Whom to Treat
There is evidence obtained from robust randomized controlled trials (RCT) that treatment improves symptoms, sleepiness, driving, cognition, mood, quality of life, and blood pressure in patients who have an Epworth score of >11, troublesome sleepiness while driving or working, and >15 apneas + hypopneas per hour of sleep. For those with similar degrees of sleepiness and 5–15 events per hour of sleep, RCTs indicate improvements in symptoms, including subjective sleepiness, with less strong evidence indicating gains in cognition and quality of life. There is no evidence of blood pressure improvements in this group, nor is there is evidence that treating nonsleepy subjects improves their symptoms, function, or blood pressure. Thus, treatment cannot be advocated for this large group.
How to Treat
All patients diagnosed with OSAHS should have the condition and its significance explained to them and to their partner. This should be accompanied by provision of written and/or web-based information and a discussion of the implications of the local regulations for driving. Rectifiable predispositions should be discussed; this often includes weight loss and sometimes reduction of alcohol consumption to reduce caloric intake and because alcohol acutely decreases upper-airway dilating muscle tone, thus predisposing to obstructed breathing. Sedative drugs, which also affect airway tone, should be carefully withdrawn.
Continuous Positive Airway Pressure (CPAP)
CPAP therapy works by blowing the airway open during sleep, usually with pressures of 5–20 cmHg. CPAP has been shown in randomized placebo-controlled trials to improve breathing during sleep, sleep quality, sleepiness, blood pressure, vigilance, cognition, and driving ability, as well as mood and quality of life in patients with OSAHS. However, this is obtrusive therapy, and care must be taken to explain the need for the treatment to the patient and his/her partner, and to support all patients on CPAP intensively, providing access to telephone support and regular follow-up. Initiation should include finding the most comfortable mask from the ranges of several manufacturers and trying the system for at least 30 min during the daytime to prepare for the overnight trial. An overnight monitored trial of CPAP is used to identify the pressure required to keep the patient's airway patent. The development of pressure-varying CPAP machines may make the in-lab CPAP night trial unnecessary, but treatment must be initiated in a supportive environment. Thereafter, patients can be treated with fixed-pressure CPAP machines set at the determined pressure or by a self-adjusting, intelligent CPAP device. The main side effect of CPAP is airway drying, which can be countered using an integral heated humidifier. CPAP use, like that of all therapies, is imperfect, but around 94% of patients with severe OSAHS are still using their therapy after 5 years on objective monitoring.
Mandibular Repositioning Splint (MRS)
Also called oral devices, MRSs work by holding the lower jaw and the tongue forward, thereby widening the pharyngeal airway. MRSs have been shown in RCTs to improve OSAHS patients' breathing during sleep, daytime somnolence, and blood pressure. As there are many devices of differing design with unknown relative efficacy, these results cannot be generalized to all MRSs. Self-reports of the use of devices long-term suggest high dropout rates.
Surgery
Four forms of surgery have a role in OSAHS, although it must always be remembered that these patients have a raised perioperative risk. Bariatric surgery can be curative in the morbidly obese. Tonsillectomy can be highly effective in children but rarely in adults. Tracheostomy is curative but rarely used because of the associated morbidity; nevertheless, it should not be overlooked in extremely advanced cases. Jaw advancement surgery—particularly maxillo-mandibular osteotomy—is effective in those with retrognathia (posterior displacement of the mandible) and should be particularly considered in young and thin patients. There is no robust evidence that pharyngeal surgery, including uvulopalatopharyngoplasty (whether by scalpel, laser, or thermal techniques) helps OSAHS.
Drugs
Unfortunately, no drugs are clinically useful in the prevention or reduction of apneas and hypopneas. A marginal improvement in sleepiness in patients who remain sleepy despite CPAP can be produced by modafinil, but the clinical value is debatable and the financial cost significant.
Choice of Treatment
CPAP and MRS are the two most widely used and best evidence-based therapies. Direct comparisons in RCTs indicate better outcomes with CPAP in terms of apneas and hypopneas, nocturnal oxygenation, symptoms, quality of life, mood, and vigilance. Adherence to CPAP is generally better than to an MRS, and there is evidence that CPAP improves driving, whereas there are no such data on MRSs, Thus, CPAP is the current treatment of choice. However, MRSs are evidence-based second-line therapy in those who fail CPAP. In younger, thinner patients, maxillo-mandibular advancement should be considered.
There is evidence obtained from robust randomized controlled trials (RCT) that treatment improves symptoms, sleepiness, driving, cognition, mood, quality of life, and blood pressure in patients who have an Epworth score of >11, troublesome sleepiness while driving or working, and >15 apneas + hypopneas per hour of sleep. For those with similar degrees of sleepiness and 5–15 events per hour of sleep, RCTs indicate improvements in symptoms, including subjective sleepiness, with less strong evidence indicating gains in cognition and quality of life. There is no evidence of blood pressure improvements in this group, nor is there is evidence that treating nonsleepy subjects improves their symptoms, function, or blood pressure. Thus, treatment cannot be advocated for this large group.
How to Treat
All patients diagnosed with OSAHS should have the condition and its significance explained to them and to their partner. This should be accompanied by provision of written and/or web-based information and a discussion of the implications of the local regulations for driving. Rectifiable predispositions should be discussed; this often includes weight loss and sometimes reduction of alcohol consumption to reduce caloric intake and because alcohol acutely decreases upper-airway dilating muscle tone, thus predisposing to obstructed breathing. Sedative drugs, which also affect airway tone, should be carefully withdrawn.
Continuous Positive Airway Pressure (CPAP)
CPAP therapy works by blowing the airway open during sleep, usually with pressures of 5–20 cmHg. CPAP has been shown in randomized placebo-controlled trials to improve breathing during sleep, sleep quality, sleepiness, blood pressure, vigilance, cognition, and driving ability, as well as mood and quality of life in patients with OSAHS. However, this is obtrusive therapy, and care must be taken to explain the need for the treatment to the patient and his/her partner, and to support all patients on CPAP intensively, providing access to telephone support and regular follow-up. Initiation should include finding the most comfortable mask from the ranges of several manufacturers and trying the system for at least 30 min during the daytime to prepare for the overnight trial. An overnight monitored trial of CPAP is used to identify the pressure required to keep the patient's airway patent. The development of pressure-varying CPAP machines may make the in-lab CPAP night trial unnecessary, but treatment must be initiated in a supportive environment. Thereafter, patients can be treated with fixed-pressure CPAP machines set at the determined pressure or by a self-adjusting, intelligent CPAP device. The main side effect of CPAP is airway drying, which can be countered using an integral heated humidifier. CPAP use, like that of all therapies, is imperfect, but around 94% of patients with severe OSAHS are still using their therapy after 5 years on objective monitoring.
Mandibular Repositioning Splint (MRS)
Also called oral devices, MRSs work by holding the lower jaw and the tongue forward, thereby widening the pharyngeal airway. MRSs have been shown in RCTs to improve OSAHS patients' breathing during sleep, daytime somnolence, and blood pressure. As there are many devices of differing design with unknown relative efficacy, these results cannot be generalized to all MRSs. Self-reports of the use of devices long-term suggest high dropout rates.
Surgery
Four forms of surgery have a role in OSAHS, although it must always be remembered that these patients have a raised perioperative risk. Bariatric surgery can be curative in the morbidly obese. Tonsillectomy can be highly effective in children but rarely in adults. Tracheostomy is curative but rarely used because of the associated morbidity; nevertheless, it should not be overlooked in extremely advanced cases. Jaw advancement surgery—particularly maxillo-mandibular osteotomy—is effective in those with retrognathia (posterior displacement of the mandible) and should be particularly considered in young and thin patients. There is no robust evidence that pharyngeal surgery, including uvulopalatopharyngoplasty (whether by scalpel, laser, or thermal techniques) helps OSAHS.
Drugs
Unfortunately, no drugs are clinically useful in the prevention or reduction of apneas and hypopneas. A marginal improvement in sleepiness in patients who remain sleepy despite CPAP can be produced by modafinil, but the clinical value is debatable and the financial cost significant.
Choice of Treatment
CPAP and MRS are the two most widely used and best evidence-based therapies. Direct comparisons in RCTs indicate better outcomes with CPAP in terms of apneas and hypopneas, nocturnal oxygenation, symptoms, quality of life, mood, and vigilance. Adherence to CPAP is generally better than to an MRS, and there is evidence that CPAP improves driving, whereas there are no such data on MRSs, Thus, CPAP is the current treatment of choice. However, MRSs are evidence-based second-line therapy in those who fail CPAP. In younger, thinner patients, maxillo-mandibular advancement should be considered.
Thursday, March 18, 2010
Treatment & Prognosis of Asthma
Treatment :
Asthma is a long-term disease that can't be cured. Every asthmatic child must have an asthma action plan.
Examples of quick relief asthma medicines include:
Although it is a chronic disease, the prognosis is usually GOOD =)
This is especially in children who only had mild attacks of asthma.
54% of cases in children will no longer carry the symptoms after a decade (10 years).
Overall, studies shown that 94% of the asthmatic adults survived the follow up period of eight years.
Asthma is a long-term disease that can't be cured. Every asthmatic child must have an asthma action plan.
Basically, there are two types of medications:
- Controller Asthma Medicines - prophylaxis
- Quick Relief Asthma Medicines - during asthma attack
Controller Asthma Medicines
Examples of controller or preventative asthma medicines include:- Inhaled corticosteroids such as Aerobid, Asmanex, Azmacort, Flovent HFA, Pulmicort (available as a Turbuhaler an Respules for use with nebulizers for younger kids), and Qvar
- Advair, a combination corticosteroid and long-acting beta2 agonist
- Leukotriene receptor antagonists, such as Singulair, Accolate, and Zyflo
- Long-acting beta2 agonists, such as Serevent Diskus and Foradil
- Theophylline
- Other non-steroidal anti-inflammatory controller asthma medications include Intal and Tilade.
- Xolair injections for children with allergic asthma.
Quick Relief Asthma Medicines
These types of asthma treatment actually provide relief when your child has asthma symptoms. They are usually given with a NEBULIZER OR A METERED DOSE INHALER. Younger children can often use an inhaler with a spacer or a spacer and mask.Examples of quick relief asthma medicines include:
- Albuterol - Accuneb, Albuterol, Proventil, Ventolin (inhalation solution, nebules, HFA inhaler, inhaler, syrup, rotacaps)
- Levaluterol - Xopenex Soln, Xopenex HFA
- Pirbuterol - Maxair Autohaler (a breath-actuated metered dose inhaler)
- Terbutaline
- Atrovent
Prognosis of Asthma
Although it is a chronic disease, the prognosis is usually GOOD =)
This is especially in children who only had mild attacks of asthma.
54% of cases in children will no longer carry the symptoms after a decade (10 years).
Overall, studies shown that 94% of the asthmatic adults survived the follow up period of eight years.
Monday, March 8, 2010
Digoxin
Digoxin
It is also known as digitalis and is extracted from the plant Digitalis lanata which is found in Eastern Europe.
Other names: Lanoxin, Digitek, and Lanoxicaps. It is also available as a 0.05 mg/mL oral solution and 0.25 mg/mL or 0.5 mg/mL injectable solution.
Its main cardiac effects are
• Negatively chronotropic - i.e. slowing the heart rate by decreasing conduction of electrical impulses through the AV node, making it a commonly used antiarrhythmic agent in controlling the heart rate during atrial fibrillation or atrial flutter.
• Positively inotropic - i.e. increasing the force of heart contraction via inhibition of the Na+/K+ ATPase pump
ATPase controls movement of calcium, sodium and potassium into heart muscle. Calcium controls the force of contraction. Inhibiting ATPase increases calcium in heart muscle and therefore increases the force of heart contractions.
Digoxin is usually given by mouth, but can also be given by IV injection in urgent situations (the IV injection should be slow, heart rhythm should be monitored). The half life is about 36 hours; digoxin is given once daily, usually in 125 μg or 250 μg dosing. Following drug administration, a 6- to 8-hour tissue distribution phase is observed.
This half life is only present for those with normal renal function, as this drug is metabolized through the kidneys.
Digoxin blood levels are used for adjusting doses in order to avoid toxicity. The usual starting dose is 0.0625-0.25 mg daily depending on age and kidney function. The dose may be increased every two weeks to achieve the desired response.
Side Effects:
Common side effects include nausea, vomiting, headache, dizziness, skin rash, and mental changes. Many digoxin side effects are dose dependent and happen when blood levels are over the narrow therapeutic range. Visual disturbances (blurred vision or yellow/green halos around objects), fast/slow/irregular heartbeat and overdosage may occur if patient is dehydrated.
It is also known as digitalis and is extracted from the plant Digitalis lanata which is found in Eastern Europe.
Other names: Lanoxin, Digitek, and Lanoxicaps. It is also available as a 0.05 mg/mL oral solution and 0.25 mg/mL or 0.5 mg/mL injectable solution.
Its main cardiac effects are
• Negatively chronotropic - i.e. slowing the heart rate by decreasing conduction of electrical impulses through the AV node, making it a commonly used antiarrhythmic agent in controlling the heart rate during atrial fibrillation or atrial flutter.
• Positively inotropic - i.e. increasing the force of heart contraction via inhibition of the Na+/K+ ATPase pump
ATPase controls movement of calcium, sodium and potassium into heart muscle. Calcium controls the force of contraction. Inhibiting ATPase increases calcium in heart muscle and therefore increases the force of heart contractions.
Digoxin is usually given by mouth, but can also be given by IV injection in urgent situations (the IV injection should be slow, heart rhythm should be monitored). The half life is about 36 hours; digoxin is given once daily, usually in 125 μg or 250 μg dosing. Following drug administration, a 6- to 8-hour tissue distribution phase is observed.
This half life is only present for those with normal renal function, as this drug is metabolized through the kidneys.
Digoxin blood levels are used for adjusting doses in order to avoid toxicity. The usual starting dose is 0.0625-0.25 mg daily depending on age and kidney function. The dose may be increased every two weeks to achieve the desired response.
Side Effects:
Common side effects include nausea, vomiting, headache, dizziness, skin rash, and mental changes. Many digoxin side effects are dose dependent and happen when blood levels are over the narrow therapeutic range. Visual disturbances (blurred vision or yellow/green halos around objects), fast/slow/irregular heartbeat and overdosage may occur if patient is dehydrated.
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