Channel: Medical collection
Forwarded from Med Fire (Dr.abdulrhman faisal)
πiron therapy in anaemia with CKD:
βοΈNICE guidelines : Diagnostic tests to determine iron status and predict response to iron therapy in anaemia with CKD
β Do it every 3 months (1β3 months for people receiving haemodialysis).
β Use percentage of hypochromic red blood cells (% HRC; more than 6%), but only if processing of blood sample is possible within 6 hours.
β If using % HRC is not possible, use reticulocyte Hb content (CHr; less than 29 pg)
β If these tests are not available or the person has thalassaemia or thalassaemia trait, use a combination of transferrin saturation (less than 20%) and serum ferritin measurement (less than 100 micrograms/litre)
β Do not request transferrin saturation or serum ferritin measurement alone to assess iron deficiency status in people with anaemia of CKD.
βοΈNICE guidelines : Diagnostic tests to determine iron status and predict response to iron therapy in anaemia with CKD
β Do it every 3 months (1β3 months for people receiving haemodialysis).
β Use percentage of hypochromic red blood cells (% HRC; more than 6%), but only if processing of blood sample is possible within 6 hours.
β If using % HRC is not possible, use reticulocyte Hb content (CHr; less than 29 pg)
β If these tests are not available or the person has thalassaemia or thalassaemia trait, use a combination of transferrin saturation (less than 20%) and serum ferritin measurement (less than 100 micrograms/litre)
β Do not request transferrin saturation or serum ferritin measurement alone to assess iron deficiency status in people with anaemia of CKD.
πtreatment fever in infant and children
β If the temperature remains elevated and the child's discomfort is not improved three to four hours after administration of acetaminophen or ibuprofen some experts suggest switching from acetaminophen to ibuprofen or ibuprofen to acetaminophen
#Uptodate2024
β If the temperature remains elevated and the child's discomfort is not improved three to four hours after administration of acetaminophen or ibuprofen some experts suggest switching from acetaminophen to ibuprofen or ibuprofen to acetaminophen
#Uptodate2024
π atrial fibrillation with acute heart failure treatment
β A) If the dysrhythmia is the cause of heart failure with hemodynamic instability β‘οΈ Immediate synchronized electrical cardioversion
β B If the dysrhythmia is in the setting of an acute heart failure exacerbation, β‘οΈcardioversion can be harmful
βAdministration of a betaβblocker or calcium channel blocker in the acute setting can worsen clinical status and should be done with caution
β Digoxin recommended by some clinicians (250βmcg IV dose)
#Accp
β A) If the dysrhythmia is the cause of heart failure with hemodynamic instability β‘οΈ Immediate synchronized electrical cardioversion
β B If the dysrhythmia is in the setting of an acute heart failure exacerbation, β‘οΈcardioversion can be harmful
βAdministration of a betaβblocker or calcium channel blocker in the acute setting can worsen clinical status and should be done with caution
β Digoxin recommended by some clinicians (250βmcg IV dose)
#Accp
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Trousseau's sing
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πMedications that may increase the risk of bleeding or bruising
β Anticoagulants
β‘οΈInterfere with clot formation (secondary hemostasis)
β Antiplatelet agents, including NSAIDsβ‘οΈInterfere with platelet function (primary hemostasis)
β Glucocorticoids β‘οΈInterfere with vascular integrity
β Antibiotics
β‘οΈCause vitamin K deficiency, especially with longer use
Some interfere with platelet function
β SSRIsβ‘οΈInterfere with platelet function (primary hemostasis)
β Vitamin Eβ‘οΈInterferes with vitamin K metabolism in some individuals
#Uptodate2024
β Anticoagulants
β‘οΈInterfere with clot formation (secondary hemostasis)
β Antiplatelet agents, including NSAIDsβ‘οΈInterfere with platelet function (primary hemostasis)
β Glucocorticoids β‘οΈInterfere with vascular integrity
β Antibiotics
β‘οΈCause vitamin K deficiency, especially with longer use
Some interfere with platelet function
β SSRIsβ‘οΈInterfere with platelet function (primary hemostasis)
β Vitamin Eβ‘οΈInterferes with vitamin K metabolism in some individuals
#Uptodate2024
#Treatment_of_Metabolic_Alkalosis:
Cause treated
IV 0.9% saline solution for chloride-responsive metabolic alkalosis
Underlying conditions are treated, with particular attention paid to correction of hypovolemia and hypokalemia.
Patients with chloride-responsive metabolic alkalosis are given 0.9% saline solution IV; infusion rate is typically 50 to 100 mL/hour greater than urinary and other sensible and insensible fluid losses until urinary Cl rises to > 25 mEq/L (> 25 mmol/L) and urinary pH normalizes after an initial rise from bicarbonaturia.
Patients with chloride-unresponsive metabolic alkalosis rarely benefit from rehydration alone.
Patients with severe metabolic alkalosis (eg, pH > 7.6) sometimes require more urgent correction of blood pH. Hemofiltration or hemodialysis is an option, particularly if volume overload and renal dysfunction are present. Acetazolamide 250 to 375 mg orally or IV once or twice a day increases HCO3β excretion but may also accelerate urinary losses of K+ and phosphate (PO4β); volume-overloaded patients with diuretic-induced metabolic alkalosis and those with posthypercapnic metabolic alkalosis may especially benefit.
In patients with severe metabolic alkalosis (pH > 7.6) and kidney failure who otherwise cannot or should not undergo dialysis, hydrochloric acid in a 0.1 to 0.2 normal solution IV is safe and effective but must be given through a central catheter because it is hyperosmotic and scleroses peripheral veins. Dosage is 0.1 to 0.2 mmol/kg/hour. Frequent monitoring of ABGs and electrolytes is needed.
#ICU note
Cause treated
IV 0.9% saline solution for chloride-responsive metabolic alkalosis
Underlying conditions are treated, with particular attention paid to correction of hypovolemia and hypokalemia.
Patients with chloride-responsive metabolic alkalosis are given 0.9% saline solution IV; infusion rate is typically 50 to 100 mL/hour greater than urinary and other sensible and insensible fluid losses until urinary Cl rises to > 25 mEq/L (> 25 mmol/L) and urinary pH normalizes after an initial rise from bicarbonaturia.
Patients with chloride-unresponsive metabolic alkalosis rarely benefit from rehydration alone.
Patients with severe metabolic alkalosis (eg, pH > 7.6) sometimes require more urgent correction of blood pH. Hemofiltration or hemodialysis is an option, particularly if volume overload and renal dysfunction are present. Acetazolamide 250 to 375 mg orally or IV once or twice a day increases HCO3β excretion but may also accelerate urinary losses of K+ and phosphate (PO4β); volume-overloaded patients with diuretic-induced metabolic alkalosis and those with posthypercapnic metabolic alkalosis may especially benefit.
In patients with severe metabolic alkalosis (pH > 7.6) and kidney failure who otherwise cannot or should not undergo dialysis, hydrochloric acid in a 0.1 to 0.2 normal solution IV is safe and effective but must be given through a central catheter because it is hyperosmotic and scleroses peripheral veins. Dosage is 0.1 to 0.2 mmol/kg/hour. Frequent monitoring of ABGs and electrolytes is needed.
#ICU note
#Treatment_of_Respiratory_Alkalosis:
Treatment of underlying disorder
Treatment is directed at finding and treating the underlying disorder. Respiratory alkalosis itself is not life threatening, so no interventions to lower pH are necessary. Increasing inspired carbon dioxide through rebreathing (such as from a paper bag) is common practice but may be dangerous in at least some patients with CNS disorders in whom the pH of cerebrospinal fluid may already be below normal.
Treatment of underlying disorder
Treatment is directed at finding and treating the underlying disorder. Respiratory alkalosis itself is not life threatening, so no interventions to lower pH are necessary. Increasing inspired carbon dioxide through rebreathing (such as from a paper bag) is common practice but may be dangerous in at least some patients with CNS disorders in whom the pH of cerebrospinal fluid may already be below normal.
πΉRespiratory alkalosis involves an increase in respiratory rate and/or tidal volume (hyperventilation).
πΉHyperventilation occurs most often as a response to hypoxia, metabolic acidosis, increased metabolic demands (eg, fever), pain, or anxiety.
πΉDo not presume anxiety is the cause of hyperventilation until more serious disorders are excluded.
πΉTreat the cause; respiratory alkalosis is not life threatening, so interventions to lower pH are unnecessary.
πΉHyperventilation occurs most often as a response to hypoxia, metabolic acidosis, increased metabolic demands (eg, fever), pain, or anxiety.
πΉDo not presume anxiety is the cause of hyperventilation until more serious disorders are excluded.
πΉTreat the cause; respiratory alkalosis is not life threatening, so interventions to lower pH are unnecessary.
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π commonly linked to #Stevens-Johnson_syndrome :
πΉAllopurinol
πΉcarbamazepine
πΉlamotrigine
πΉnevirapine
πΉoxicam anti-inflammatories, such as meloxicam and piroxicam
πΉphenobarbital
πΉphenytoin
πΉsulfamethoxazole and other sulfa antibiotics
πΉsulfasalazine
#Note:
In children, Stevens-Johnson syndrome can sometimes be caused by infections like cold or flu, cold sores and glandular fever.
πΉAllopurinol
πΉcarbamazepine
πΉlamotrigine
πΉnevirapine
πΉoxicam anti-inflammatories, such as meloxicam and piroxicam
πΉphenobarbital
πΉphenytoin
πΉsulfamethoxazole and other sulfa antibiotics
πΉsulfasalazine
#Note:
In children, Stevens-Johnson syndrome can sometimes be caused by infections like cold or flu, cold sores and glandular fever.
#Note :
If a woman is BRCA positive or has β₯2 first-degree relatives, give tamoxifen or an aromatase inhibitor for 5 years starting age 35.
This primary prevention cuts the risk of breast cancer by 50%.
If a woman is BRCA positive or has β₯2 first-degree relatives, give tamoxifen or an aromatase inhibitor for 5 years starting age 35.
This primary prevention cuts the risk of breast cancer by 50%.
βοΈMetabolic Acidosis Causes
"KUSSMAL"
πΉKetoacidosis
πΉUremia
πΉSepsis
πΉSalicylates
πΉMethanol
πΉAlcohol
πΉLactic Acidosis.
"KUSSMAL"
πΉKetoacidosis
πΉUremia
πΉSepsis
πΉSalicylates
πΉMethanol
πΉAlcohol
πΉLactic Acidosis.
π§§Type Of Metabolic acidosis:
1-Normal anion gap
Mechanism :-
β’ Loss of bicarbonate
Etiologies :-
β’ Severe diarrhea
β’ Renal tubular acidosis
β’ Excesssaline infusion
β’ Intestinal or pancreatic fistula
β’ CAI & MRA diuretics
2 -Elevated anion gap
Mechanism :-
β’ Accumulation of unmeasured acidic compounds
Etiologies :-
β’ Lactic acidosis
β’ Diabetic ketoacidosis
β’ Renal failure (uremia)
β’ Methanol, ethylene glycol
β’ Salicylate toxicity.
1-Normal anion gap
Mechanism :-
β’ Loss of bicarbonate
Etiologies :-
β’ Severe diarrhea
β’ Renal tubular acidosis
β’ Excesssaline infusion
β’ Intestinal or pancreatic fistula
β’ CAI & MRA diuretics
2 -Elevated anion gap
Mechanism :-
β’ Accumulation of unmeasured acidic compounds
Etiologies :-
β’ Lactic acidosis
β’ Diabetic ketoacidosis
β’ Renal failure (uremia)
β’ Methanol, ethylene glycol
β’ Salicylate toxicity.
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