🤓MNEMO>

Do you know what CVS anomaly you have to rule out, if you get a patient with TURNERS SYNDROME, for any surgery?

😉Aorta is the vessel, which 'TURNs back'😉

Answer: Coarctation of Aorta, Aortic Valvular Disease❗️

#mnemonic ,#MedicalMnemonic

BLOODY MATCH MAKING❗️❗️❗️❗️

💋RED CELL COMPONENTS 

In red cell transfusion, there must be ABO and RhD compatibility between the donor’s red cells and the recipient’s plasma. 

❤️Group O individuals can receive blood from group O donors only 

❤️Group A individuals can receive blood from group A and O donors 

❤️Group B individuals can receive blood from group B and O donors 

❤️Group AB individuals can receive blood from AB donors, and also from group A, B and O donors

(Red cell concentrates, from which the plasma has been removed, are preferable when non-group specific blood is being transfused.)

💋PLASMA AND COMPONENTS CONTAINING PLASMA 

In plasma transfusion, group AB plasma can be given to a patient of any ABO group because it contains neither anti-A nor anti-B antibody. 

❤️Group AB plasma (no antibodies) can be given to any ABO group patients 

❤️Group A plasma (anti-B) can be given to group O and A patients 

❤️Group B plasma (anti-A) can be given to group O and B patients 

❤️Group O plasma (anti-A + anti-B) can be given to group O patients only

Reference:

THE CLINICAL USE OF BLOOD: HAND BOOK , World Health Organization & Blood Transfusion Safety , GENEVA 

#blood , #transfusion , #TransfusionMedicine ,#BloodCompatibility ,#BloodTransfusion ,#anesthesia ,#BloodDonor ,#BloodBank

BREAK THE CAMOUFLAGE ⚒ 👹DIABETES INSIPIDUS Vs 👺SIADH Vs 🤖CSWS

DIABETES INSIPIDUS (DI)

➖➖➖➖➖➖➖➖➖

🧀Absence/ ineffectiveness of ADH to concentrate urine 

🧀Leads to the passage of a large volume of inappropriately dilute urine with a consequent rise of plasma osmolality (due to disproportionate loss of water over sodium) and progressive dehydration. 

DIAGNOSIS

🧀DI is present when the urine output is excessive, the urine osmolality is inappropriately low relative to serum osmolality (which is above normal because of water loss), and the urine specific gravity is less

🧀Polyuria (more than 4 ml/kg/hr in children, more than 6 ml/kg/hr in neonates or, in an adult >250 mL/hour or 4 to 14 L/day) of dilute urine 

🧀Dehydration

🧀Hypernatremia

🧀increased serum osmolality (>295 mOsm/kg)

🧀decreased urine osmolality (<300 mOsm/kg)

🧀decreased urine specific gravity (<1.002-1.005)

TREATMENT 

Hydration

🧀The amount and content of intravenous fluids are guided by urine volume, serum electrolytes and serum osmolality. 

🧀 If fluid is replaced early, it is not necessary to administer free water (D5W). Rather, a hypotonic solution such as 0.45% sodium chloride (NaCl) or lactated Ringer's may be given. 

🧀 Insulin and potassium supplementation might be required when dextrose-containing fluids are used, especially if corticosteroids are used concomitantly. Give appropriate potassium supplementation. 

Hormonal 

🧀 If the urine output is >250-300 mL/hour for 2 hours hormonal treatment is given

🧀 Desmopressin (DDAVP), a synthetic analog of the natural hormone arginine vasopressin, is available as intranasal, oral, or IV forms. 

✔️The intranasal preparation of DDAVP delivers a 10 ug dose per spray, and doses of 10-30 ug per day are usually effective. 

✔️The IV form (4 ug/mL) is given IV, intramuscularly (IM), or subcutaneously in doses of 0.5–2 ug every 8–12 hours as needed. 

✔️Oral tablets (0.1–0.2 mg) in doses of 0.1–1.2 mg/day can also be given to obtain adequate diuresis.

✔️Vasopressin can be given subcutaneously in doses of 4–10 units every 6 hours as needed for urine output exceeding 250 mL.

✔️Alternatively, a continuous infusion can be used, as the half-life of vasopressin given IV is only 20 minutes. A dose of 0.008 – 0.04 units/kg/hour is usually effective

🧀 Once intravascular volume has been restored, persistent hypernatremia may be treated with thiazide diuretics, such as hydrochlorothiazide, 50 to 100 mg/day i.v.

Syndrome of inappropriate antidiuretic hormone secretion (SIADH). 

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🧀Various cerebral pathologic processes (mostly head trauma) can cause excessive release of ADH, which leads to the continued renal excretion of sodium (>20 mEq/L), despite hyponatremia and associated hypo osmolality. 

🧀 The key findings are urinary sodium loss without corresponding loss of water, leading to a decrease in plasma osmolality in the presence of hypertonic urine. 

Urine osmolality is therefore high relative to serum osmolality. 

🧀 Blood urea nitrogen (BUN) and serum creatinine are normal and serum uric acid is generally low.

TREATMENT 

🧀 The mainstay is fluid restriction to 1,000 mL/24 hours of iso-osmolar solution. 

🧀 If hyponatremia is severe (<110 to 115 mEq/L), the administration of hypertonic (3% to 5%) saline and furosemide might be appropriate. Because rapid correction of hyponatremia has been associated with the occurrence of central pontine myelinolysis, restoring serum sodium at a rate of approximately 2 mEq/L/hour is advisable.

Cerebral Salt Wasting Syndrome (CSWS)

➖➖➖➖➖➖➖➖➖➖➖➖➖➖

🧀 It is renal loss of sodium due to intracranial disease, leading to hyponatremia and hypovolemia. 

🧀 Raised levels of circulating ANP and BNP mediate, increased natriuresis and hyponatremia in acute brain injury

🧀 CSWS is predominantly associated with SAH but has also been described in conjunction with TBI, glioma, and tuberculous or carcinomatous meningitis.

🧀 The key distinction to be made is that patients with CSWS are clinically hypovolemic compared with the euvolemic or slightly hypervolemic status of patients with SIADH. Patients with CSWS may have abnormally elevated BUN greater than creatinine, increased hematocrit, and increased serum uric acid.

DO U KNOW❓

🧀 Hypothyroidism is another important consideration in patients with hyponatremia following pituitary surgery. It may even occur in patients who are partially treated. 

🧀 decreased cardiac output (with stimulation of baroreceptors leading to increased ADH release), decreased clearance of ADH, or resetting of the osmostat may all contribute (ref : Postoperative Care Following Pituitary Surgery, Journal of Intensive Care Medicine 20(3); 2005, P:134)

ADDITIONAL EXPLANATION: DI

🧀 In neurologic practice, it is particularly associated with pituitary surgery,Traumatic Brain Injury and anterior communicating artery aneurysmal SAH.Patients who become brain dead often develop severe DI and this is relevant in the management of potential organ donors.

🧀 Diuresis of solute may also be caused by osmotic diuresis secondary to the use of mannitol or hypertonic saline, for control of intracranial pressure, or hyperglycemia.

🧀 DONT DO THIS❗️Excess fluids are sometimes administered intravenously during the perioperative period, which are then excreted appropriately postoperatively. If this large postoperative diuresis is matched with continued intravenous fluid infusions, an incorrect diagnosis of DI may be made based on the resulting hypotonic polyuria. Therefore, if the serum [Na] is not elevated concomitantly with the polyuria, the rate of parenterally administered fluid should be slowed with careful monitoring of the serum [Na] and urine output until a diagnosis of DI can be confirmed by continued hypotonic polyuria in the presence of hypernatremia or hyperosmolality.

ADDITIONAL EXPLANATION: SIADH

🧀 The most common causes in the neurologic group include meningitis/encephalitis, brain tumor, SAH, and TBI. 

🧀 Also reported following spinal surgery.

🧀 Drug-related hyponatremia secondary to the antiepileptic drugs carbamazepine and  oxcarbamazepine 

#anaesthesia ,#neurosurgery , #endocrinology ,#pituitary , #DiabetesInsipidus , #desmopressin , #siadh 

REFERENCE:

Endocrinol Metab Clin N Am 37 (2008) 213–234Disorders of Water and Salt Metabolism Associated with Pituitary Disease Jennifer A., Joseph G. Verbalis

Newfield, Philippa; Cottrell, James E., Handbook of Neuroanesthesia, 4th Edition

Disturbances of Sodium in Critically Ill Adult Neurologic Patients A Clinical Review Martin Tisdall, MRCS, Matthew Crocker,Jonathan Watkiss and Martin Smith, (J Neurosurg Anesthesiol 2006;18:57–63)

REFINE YOUR IMPRESSION OF 📕PaO2 Vs 📗SaO2 Vs 📘CaO2

⭕️Oxygen content ( PaO2 )  is the pressure of oxygen molecules dissolved in blood, and is measured by ABG analysis with units of kPa or mmHg 

⭕️Oxygen saturation ( SaO2 )  is a measure of the percentage of haemoglobin sites that have oxygen bound, commonly measured with a pulse oximeter 

⭕️Oxygen content ( CaO2 )   is the real measure of blood oxygen quantity as it accounts for dissolved and haemoglobin bound oxygen. (i.e. CaO2 directly reflects the TOTAL number of oxygen molecules in arterial blood, both bound and unbound to hemoglobin.  It is given as the volume of oxygen carried in each 100 ml blood (mL O 2 /100 mL). Normal CaO2 ranges from 16 to 22 ml O2/dl.

EXPLANATION:

⭕️Oxygen saturation ( SaO2 ) is expressed as the percentage of haemoglobin-binding sites that are occupied by oxygen, thereby forming oxyhaemoglobin. 

⭕️Arterial blood is normally at 97–98% O 2  saturation (i.e. 98% of the available haemoglobin is combined with O 2 ), whereas venous blood is normally at 74% O2  saturation. 

⭕️O2 constitutes 21% of the atmosphere by volume and atmospheric PO2 is 159 mmHg at sea level . At an alveolar pressure of 104 mmHg, alveolar oxygen diffuses into pulmonary venous blood and raises its O2 content from 15 mL/100 mL to 20 mL/100 mL. Of this amount 19.75 mL is combined with haemoglobin and 0.25 mL is ‘free’ or dissolved in simple solution in the plasma. At this pressure of alveolar O2 , haemoglobin in the arterial blood normally becomes 98% saturated and and 2% of the haemoglobin remains reduced, i.e. free of oxygen.

⭕️PaO2 is determined by alveolar PO2 and the state of the alveolar-capillary interface, not by the amount of hemoglobin available to soak them up. PaO2 is not a function of hemoglobin content or of its characteristics. This explains why, for example, patients with severe anemia or carbon monoxide poisoning or methemoglobinemia can (and often do) have a normal PaO2.

⭕️The most common physiologic disturbance of lung architecture, and hence of a reduced PaO2, is ventilation-perfusion (V-Q) imbalance. Less common causes are reduced alveolar ventilation, diffusion block, and anatomic right to left shunting of blood. 

⭕️Think of PaO2 as the driving pressure for oxygen molecules entering the red blood cell and chemically binding to hemoglobin; the higher the PaO2, the higher the SaO2. 

⭕️ In contrast to the other two variables, CaO2 depends on the hemoglobin content and is directly related to it; Since the dissolved oxygen contributes minimally to CaO2 under physiologic conditions, CaO2 is determined almost entirely by hemoglobin content and SaO2, and is related linearly to either variable.

CaO2 = Hb (gm/dl) x 1.34 ml O2/gm Hb x SaO2 + PaO2 x (.003 ml O2/mm Hg/dl).

#oxygen , #spo2 , #respiration , #O2 , #pulmonology , #OxygenCascade , #anaesthesia 

Reference:

(Chapter 5 of Dr. Martin's book All You Really Need to Know to Interpret Arterial Blood Gases, 2nd edition, published February 1999 by Lippincott Williams & Wilkins, Understanding ABGs & Lung Function Tests,Pocket Tutor, Muhunthan  Thillai ,Keith Hattotuwa )

COME ON B.P.😲😲😲😲😲😲‼️

✔️The specific intraoperative situations in which induced arterial hypertension might be beneficial in Neuroanesthesia : 

(1) interventional neuroradiology (e.g.endovascular obliteration of cerebral aneurysms, cerebral angioplasty/stenting and intraarterial thrombolysis; 

(2) transient vessel occlusion during clipping of cerebral aneurysm and carotid endarterectomy

(3) extracranial to intracranial bypass surgery

(4) Surgery in patients with cerebral vasospasm after subarachnoid haemorrhage 

(5) In patients with a change in the cerebral autoregulation relationship, (e.g. intracranial pathology with mass effect, systemic hypertensive disease and traumatic brain injury.)

✔️Increase in BP is attained by vasoconstriction (rather than by increasing the cardiac output because changes in cardiac output do not affect CBF.)

✔️So intraoperatively alpha-agonist, phenylephrine is commonly used. 

✔️Others like dopamine, dobutamine and vasopressin can be used in the ICU.

#InducedHypertension , #NeuroAnaesthesia , #neurosurgery , #sah , #stroke , #anesthesia , #anaesthesia , #neurointensivecare , #criticalcare 

Reference:

Curr Opin Anesthesiol 2012, 25:548–555

Protecting the brain during neurosurgical procedures: strategies that can work, Hossam El Beheiry

👁➖BE AWARE OF AWARENESS ➖👁

💣Premeditation  with amnestic reduces the chance of awareness. Also, if awareness occurs, psychological trauma is less likely without recall. 

💣Light induction doses and liberal use of muscle relaxants ,without giving adequate concern to the depth of anaesthesia can increase the chance of awareness.

💣Better to give re-bolus with i.v. hypnotic during multiple intubation attempts. Consider using inhalation induction technique. 

💣Beta-blockers,can reduce MAC-Awake and may also decrease the likelihood of PTSD. 

💣We can consider ear plugs or headphones to reduce awareness of noises in the OR. 

💣Nitrous oxide, Ketamine and Opioids suppress cortical arousal during painful stimulation, which may reduce the probability of awareness. But BIS and other EEG monitors do not accurately predict the depth of anesthesia with these drugs. (Because, even though they produce hypnosis, they do not modulate GABA-A receptors and are associated with unchanged or increased high frequency EEG signals.)

💣Propofol, barbiturates, etomidate, and halogenated volatile anesthetic agents all modulate GABA-A receptor activity and shift the cortical EEG to lower frequencies. So, BIS and other EEG-based monitors provide strong correlation with hypnosis for this group of general anesthetics.

💣MAC for N2O & volatile anesthetics is additive (i.e. a mixture of 0.5 MAC N2O plus 0.5 MAC volatile suppresses movement in response to pain like 1 MAC volatile. The HYPNOTIC activities of nitrous oxide and volatile anesthetics are sub-additive. (i.e. a mixture of 0.5 MAC-awake N2O + 0.5 MAC-awake volatile anesthetic is not as hypnotic as 1 MAC-awake volatile. This suggests that N2O has an action which antagonizes the hypnosis induced by volatile anesthetics, perhaps via direct cortical arousal.

💣Many studies say, BIS is not useful in case of dexmedetomidine also; while some others say it will help.

#awareness , #anesthesia , #sedation , #AwarenessAnesthesia , #bis , #AwarenessSurgery 

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Reference:

 CampagnaJA,MillerKW,FormanSA:Mechanismsofactionsof inhaled anesthetics. N Engl J Med 348:2110-2124, 2003

SleighJW,BarnardJP:Entropyisblindtonitrousoxide.Canwesee why? Br J Anaesth 92:159-161, 2004 39. 

ChortkoffBS,BennettHL,EgerEI2nd:Doesnitrousoxideantagonize isoflurane-induced suppression of learning? Anesthesiology 79: 724-732, 1993 40. 

KatohT,IkedaK,BitoH:Doesnitrousoxideantagonizesevofluraneinduced hypnosis? Br J Anaesth 79:465-468, 1997

Update on Bispectral Index monitoring Jay W. Johansen,Best Practice & Research Clinical Anaesthesiology Volume 20, Issue 1, March 2006, Pages 81–99

LAB et al.....(Started working).....LOL😆😆😆😆 labetalol SAGA

〰〰〰〰〰〰〰〰〰〰〰〰〰〰〰〰〰〰

💉Comes as 5  mg/mL  ampoules 

💉Infusion:  200 mg/200  mL 

     Add  200mg  [40  mL]  labetalol  to  160  mL  D5W,      NS,  LR,  or  D5/NS 

     Final  concentration:  1  mg/mL 

💉Blocks  α,  β1,  and  β2  adrenergic  receptor  sites.    

💉Decreases  heart  rate  and  peripheral  vascular  resistance.  

💉Ratio  of  alpha-‐  to  beta-‐ blockade  depends  upon  the  route  of  administration  (1:3  oral  versus  1:7  IV)  

💉Onset  of  action:  2-‐ 5  minutes  

💉Duration:  2-‐ 4  hours

💉IV  Bolus:  20  mg  over  at  least  2  minutes  as  initial  dose, may  repeat  with  doses  of  40-‐ 80  mg  q10min; Do  not  exceed  total  dose of 300 mg 

💉 Infusion:  starting  2  mg/min  (2  mL/min)  –  8  mg/min  titrated  to  response.   Do  not  exceed  total  dose  of  300

💉As  cumulative  dose  nears  300mg  IV,  duration  of  action  extends  to  nearly  18  hours.

🙀-NEW INSIGHTS: 

Antihypertensive drugs methyldopa, labetalol, hydralazine, and clonidine improve trophoblast interaction with endothelial cellular networks in vitro

B Xu, F Charlton, A Makris, A Hennessy - Journal of hypertension, 2014 

#anesthesia , #GDM , #PIH , #anaesthesia

BASIC INFO: Guillain-Barre Syndrome in Neuro Critical Care Unit

🔵is an Acute Inflammatory Demyelinating Polyneuropathy (AIDP) 

🔵There will be diffuse weakness, areflexia and albuminocytologic dissociation. 

🔵In ~60% there can be preceding upper respiratory infection or diarrhea with 30% of these cases attributed to Campylobacter jejuni  

🔵Neurologic symptoms: numbness, paraesthesias, dysesthesias and progressive, bilateral symmetric weakness that progresses over hours to days and peaks in a few weeks. 

🔵normal or hyperreflexia in the initial phase changes to  areflexia. 

🔵CSF : elevated protein without pleocytosis (albuminocytologic dissociation is seen with only in 50% of patients during their first week of illness and up to 75% by the third week)

🔵Lumbar puncture is necessary to rule out infectious diseases and malignancies. 

🔵Medical complications : Respiratory failure and need for mechanical ventilation, aspiration pneumonia, sepsis, arrhythmias, cardiac arrest, and dysautonomia. 

🔵Screening for dysphagia and frequent bedside spirometry is necessary to prevent aspiration and further respiratory compromise. 

🔵They often require narcotics, gabapentin or carbamazepine to manage their acute pain (A small portion of patients will continue to experience radicular, arthralgia or meningitic pain up to one year later.) A dual approach of psychosocial support and SSRI therapy is recommended. 

🔵 both PLEX and IVIG are effective therapies for patients with GBS. 

🔵 Patients admitted within two weeks of symptom onset, bed bound on admission, and those that have minimal comorbidities can be considered for PLEX first. 

🔵 IVIG is may be easier to administer, especially when placement of a central line is not readily available. 

🔵 A Cochrane systematic review published in 2012 concluded that PLEX is more effective than supportive care, IVIG may be slightly safer, and combination therapy was not more effective than monotherapy 

Reference :

>Jacob S, Viegas S, Lashley D, Hilton-Jones D (2009) Myasthenia gravis and other neuromuscular junction disorders. Pract Neurol 9: 364-371. 

>Hughes RA, Swan AV, van Doorn PA (2012) Intravenous immunoglobulin for Guillain-Barré syndrome. Cochrane Database Syst Rev. Wil ey Online Library 7.

>Bedside Critical Care Guide / Ramzy H Rimawi

#GBS , #GBSICU , #PLEX, #neuroicu ,#neurology ,#anaesthesia ,#anesthesiologist

THE DICTATORS OF NIGHT👑💤; NREM Vs REM COMPARISON↔️

🎭Cerebral blood flow is reduced in NREM , whereas it is markedly increased in REM

🎭Sleep walks and night terrors occur in NREM; whereas dreams occur in REM

🎭Muscle tone, especially, Upper airway muscle tone is significantly reduced in REM. 

🎭DO YOU KNOW❓The only somatic muscles working in REM are the extraocular muscles and diaphragm❗️❗️

🎭There is a shift in the autonomic nervous system in sleep, with parasympathetic nervous system predominance in NREM and especially in REM

🎭NREM is organized into four stages. In a typical night of adult sleep, Stage 1 will comprise up to 5% of total sleep, Stage 2 up to 50%, SWS ( Slow Wave Sleep= Stage 3+4) up to 20%, and REM up to 25%

🎭SWS is predominately experienced in the first third of sleep and REM in the last half of sleep. Achieving SWS has neuroendocrine significance.

〰NEW INSIGHTS〰

😴Unlike propofol, sevoflurane anesthesia has differential effects on NREM and REM sleep homeostasis. (i.e.  Total sleep deprivation resulted in significantly increased NREM and REM sleep for 12-h postdeprivation. Sevoflurane exposure after deprivation eliminated the homeostatic increase in NREM sleep and produced a significant decrease in the NREM sleep δ power during the postanesthetic period, indicating a complete recovery from the effects of deprivation)

These data confirm the previous hypothesis that inhalational agents do not satisfy the homeostatic need for REM sleep, and that the relationship between sleep and anesthesia is likely to be agent and state specific.

(Pal D, Lipinski WJ, Walker AJ, Turner AM, Mashour GA

Anesthesiology [2011, 114(2):302-310)]

😴Help your patient in getting a quality sleep on preoperative day❗️

Sleep Loss and REM Sleep Loss are Hyperalgesic

Timothy Roehrs, Maren Hyde, Brandi Blaisdell, M Mark Greenwald, Thomas Roth (SLEEP, Vol. 29, No.2, 2006)

#sleep ,#nremsleep , #rem , #SleepClinic , #SleepStudy , #AnaesthesiaSleep ,#osas ,#cpap ,#brain , #SWS

HYPOPHOSPHATAEMIA IN ICUs🌀

🔹Normal range (2.5-4.5 mg/dL),

🔹Plasma phosphate concentration < 2.5 mg/dL or 0.81 mmol/L

CAUSES:

🔹Poor Nutrition

🔹Chronic Alcoholism

🔹Diarrhoea

🔹Beta 2 Agonists

🔹Insulin 

🔹Acetazolamide

🔹Hemodialysis 

🔹Hyperparathyroidism

EFFECTS

🔹Irritability 

🔹Confusion

🔹Metabolic encephalopathy 

🔹Coma

🔹Muscle weakness 

🔹Respiratory failure

🔹Failure to wean from ventilator

🔹Dysphagia

🔹Ileus

🔹cardiac arrhythmias and cardiomyopathy.

🔹ODC shift to left

TREATMENT

🔹Asymptomatic mild-to-moderate hypophosphatemia (1-2.5 mg/dL) can be treated with oral phosphate supplementation if the gastrointestinal tract is intact. 

🔹Symptomatic or severe hypophosphatemia (< 1.0 mg/dL) should be treated with intravenous phosphate.

🔹Oral supplementation : 2.5 to 3.5 g (80 to 110 mmol) per day, divided over two to three doses.

Intravenous:

🔹The required dose of initial intravenous phosphate may vary from 2.5 to 19.8 mg/kg.

Typically, 2-5 mg/kg of inorganic phosphate dissolved in 0.45% saline is given over 6-12 hours and repeated as needed.

🔹Rapid or large infusions are dangerous : Large intravenous doses of phosphate may result in hyperphosphatemia, hypomagnesemia, hypocalcemia, and hypotension.

🔹Hyperkalemia is prevented by using sodium phosphate instead of potassium phosphate in patients with potassium levels >4 mmol/L.

🔹Do not mix with Calcium or Magnesium

🔹Daily Phosphate level monitoring should be done

#hypophosphaetemia , #phosphorous , #electrolytes , #icu , #criticalcare , #IntensiveCare