Skip to main content

First is first

"Primum non nocere"
First, do no harm.

One of the rule of practicing good medicine, is to know precisely, what not to do, to avoid catastrophe,  to the patient as well as the physician.

●INSULIN INFUSION BEFORE CORRECTING POTASSIUM, in hyperglycemic states:
Adult patients presenting with Diabetic Ketoacidosis or Hyperosmotic hyperglycemic state, usually have total body potassium deficit of about 300-600 mEq/L. It is the result of osmotic diuresis and secondary hyperaldosteronism. Despite this serum potassium is usually normal or in one third of cases, may be elevated on admission, due primarily to insulin deficiency and hyperosmolality,  both of them drive potassium out of cells.
Insulin infusion will reverse this movement and cause dramatic fall in serum potassium concentration. Which can lead to life threatening cardiovascular and neuromuscular complications.
Therefore insulin infusion should not be started if serum Pottasium is less than 3.3 mEq/L. Potassium must be replace, and rechecked. When it has increased to more than 3.3 mEq/L, insulin infusion is started. Similarly anytime duting treatment, if serum potassium falls below 3.3 mEq/L, insulin infusion should be stopped and potassium is replaced. Insulin is resumed only when potassium rises above 3.3 mEq.
Potassium should be replaced during insulin infusion if it less than 5.3 mEq/L.

●INTRAVENOUS GLUCOSE BEFORE THIAMINE SUPPLEMENTATION, in chronic alcohol abuse and withrawl:
Thiamine is a cofactor for several enzymes in energy metabolism, including transketolase, alphaketoglutarate dehydrogenase, and pyruvate dehydrogenase. Thiamine requirement increases with high metabolic rate and high glucose intake.
Chronic alcohol abuser, develope Thiamine deficiency because of poor dietary intake, reduced gastrointestinal absorption, decreased Hepatic storage and impaired utilization.
This leads to precipitation of wernicke encephalopathy if intravenous glucose is administered before Thiamine. Therefore always administer thiamine before giving glucose in these patients.

●BETA BLOCKERS BEFORE GIVING ALPHA BLOCKERS,  to control blood pressure in Pheochromocytoma:
Pheochromocytoma is a rare catecholeamine secreting endocrine tumor.
Beta blockers should never be started first, as onopposed alpha adrenergic receptor stimulation, can further increase blood pressure.
Alpha blocker is started 10-14 days before surgery. A longer duration is required in patients with recent myocardial infarction, catecholamine cardiomyopathy,  refractory hypotension.  Beta blocker should be commenced 2-3 days before going for surgery.

●VASODIALATIRS BEFORE GIVING BETA BLOCKERS, in aortic dissection and aneurysm:
Shearing force generated by increased Aortic wall stress, will cause further propagation of intimal tear and dissection. Aortic Wall stress is determined by left ventricular contractile force, which is measured by rate of rise in LV pressure during early systole (dP/dt). dP/dt is affected by ventricular mass (muscle fibre length), and heart rate. Tachycardia increases dP/dt.
Therefore control of heart rate and blood pressure is a important measure to prevent further increase in dissection. Beta blocker should be started and titrated to target Systolic blood pressure 100-110 mmHg and heart rate less than 60 per minute.
Vasodilators must be avoided as first choice, as by causing reflex tachycardia, it will increase the shearing force (dP/dt), and propagate the dissection. Once heart rate has been controlled, vasodilators can be used to further control blood pressure.

Comments

Popular posts from this blog

FROM BICARBONATE TO STRONG ION DIFFERENCE- INTRIGUING STORY OF BLOOD ACID-BASE ANALYSIS   “Life is struggle, not against sin, not against money power…. but against Hydrogen ion.” - H.L. Mencken, 1919   Since the understanding of similarity between fermentation of wine and respiration of animals, evolution of human physiology and measurement of carbon dioxide is coupled with studies of acids and bases. Alkalinity of blood was demonstrated by color indicators as early as eighteenth century by French chemist Hilaire Marin Rouelle, and one century later, its relation with gastric acid secretion was recognized by Henry Bence Jones. In 1831, William B. O’Shaughnessy, an Irish physician working in India, demonstrated that Cholera reduced the free alkali of blood. But the discovery of relationship between blood alkalinity and carbon dioxide was contained within the mystery of diabetic coma.   1.     Story of Carbon Dioxide and Alkalinity of blood   In Nineteen...

Vocal Cord Dysfunction (VCD ) or PARADOXICAL VOCAL CORD MOVEMENT (PVCM)

▪Inappropriate adduction of true vocal cords, mostly during inspiration. This results in dyspnoea and strider during inspiration. Rarely it may happen during expiration also. ▪15 Y F presenting with acute respiratory distress for 48 hours. For the past 2 years she was on inhaled bronchodialtors and steroids with short cources of oral/IV steroids for bronchial asthma. There was history of 4 hospital admissions and several emergency visits for symptoms attributed to asthma. Examination revealed apprehensive, tachycardic, tachpnoic girl with accessory muscle use and widespread rhonchi bilaterally, SPO2 93% on room air. Other systemic examination were normal. She was started on inhalation therapy but her conditioned worsened. Oxygen saturation felled to 78% ON 10 L face mask,  ABG revealed pH 7.53, PaO2 58, PaCO2 28. She was intubated emergency and shifted TO ICU. She was treated as life threatening attack of bronchial asthma. She improved dramatically and successfully e...

REVERSE TRIGGERING: A newly classified though common form of double triggering

Reverse triggering is a recently defined type of double triggering where a controlled mechanical breath, stimulates receptors in the lung, eliciting inspiratory effort. Seen in patients who are deeply sedated with high mechanical ventilation rates. Reverse triggering could be explained by respiratory entrainment, a form of patient ventilator interaction, where diaphragmatic muscle contraction is triggered by ventilator insufflations, leading to breath initiation. Consequences of reverse triggering are large. Continuously induced muscle contraction of diaphragm cause cytokine release and muscle fibre damage. Additionally it increases inspiratory muscle load and oxygen consumption and may lead to cardiovascular instability. Reverse triggering also makes measurement of plateu pressure misleading as well as may generate high platue pressure and ventilator induced lung injury. Management is not entirely clear. Increasing sedation does not help. Increasing inspiratory time will cause the...