Sunday, November 29, 2015
Normal range (2.5-4.5 mg/dL),
Plasma phosphate concentration < 2.5 mg/dL or 0.81 mmol/L
Beta 2 Agonists
Failure to wean from ventilator
cardiac arrhythmias and cardiomyopathy.
ODC shift to left
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.
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
Saturday, November 28, 2015
COAGULATION STUDIES --> SODIUM CITRATE
PERIPHERAL SMEAR--> EDTA
Hb , PCV --> DOUBLE OXALATE
OSMOTIC FRAGILITY --> HEPARIN
BLOOD SUGAR--> SODIUM FLURIDE + OXALATE
#anticoagulants , #LabTests , #laboratary , #esr , #anaesthesia , #anaesthesiologist
Thursday, November 26, 2015
✔️Incidence up to more than 40%
✔️Might be occurring together with EEG-changes
✔️Methods usually tried to reduce the incidence: addition of nitrous oxide, premedication with benzodiazepines, early extubation, switching to other inhaled anaesthetics
✔️Propofol maintenance after sevoflurane induction seems to be the best alternative.
✔️A recent study also indicates that a switch to desflurane for maintenance after sevoflurane inhalation induction reduces the incidence of emergence agitation by 50 %
✔️ A paranoid delusion is said to be a common feature of this state of agitation.
✔️ Information about this phenomenon should be explained to the parents before the procedure.
#EmergenceDelirium , #Sevoflurane , #PostoperativeAgitation , #anaesthesia ,#Propofol
MayerJ,BoldtJ,Röhm K Detal (2006) Desflurane after Sevoflurane inhaled induction reduces severity of emergence agitation in children undergoing minor ear nose-throat surgery compared with sevoflurane induction and maintenance. Anesth Analg 102:400-404 22.
Breschan C, Platzer M, Jost R et al (2007) Midazolam does not reduce emergence delirium after sevoflurane anesthesia in children. Pediatr Anesth 17:347-352
UezonoS,GotoT,TeruiKetal(2000)Emergence agitation after sevoflurane versus propofol in pediatric patients. Anesth Analg 91:563-566 20.
NakayamaS,FurukawaH,YanaiH(2007)propofol reduces incidence of emergence agitation in preschool-aged children as well as in school-aged children: a comparison with sevoflurane. J Anesth 21:19-23
Moos DD (2005) Sevo and emergence behavioural changes in pediatrics .JPeri Anesth Nurs 20:13-18
Wednesday, November 25, 2015
SSEP reflect the ability of a specific neural pathway to conduct an electrical signal from the periphery to the cerebral cortex.
THIS IS WHAT WE DO:
A skin surface electrode is placed near a major peripheral mixed function (motor and sensory) nerve such as the median --> a square-wave electrical stimulus of 0.2 to 2ms is applied at a rate of 1 to 2Hz. --> The stimulus intensity is adjusted to produce minimal muscle contraction (usually 10 to 60mA) --> The resulting electrical potential is recorded at various points along the neural pathway from the peripheral nerve to the cerebral cortex.
COMMON SITES OF STIMULATION:
#Upper extremity : median and ulnar nerves at the wrist.
#Lower extremity : the common peroneal nerve at the popliteal fossa and the posterior tibial nerve at the ankle
#Less commonly the tongue, trigeminal nerve, and pudendal nerve have been studied.
After upper limb stimulation, potentials are recorded at the brachial plexus (Erb’s point, 2 cm superior to the clavicular head of the sternocleidomastoid muscle), the cervicomedullary junction (posterior midline of the neck at the second cervical vertebra), and the scalp overlying the somatosensory cortex on the contralateral side.
After stimulation of the lower extremity, potentials are recorded at the popliteal fossa, lumbar and cervical spinal cord, and somatosensory cortex. It is important to record nerve and subcortical potentials to verify adequate stimulation and delineate anesthetic effects.
The SSEP is plotted as a waveform of voltage vs. time.
It is characterized by:
#Amplitude (A), which is measured in microvolts from baseline to peak or peak to peak
#Latency (L), which is the time, measured in milliseconds, from onset of stimulus to occurrence of a peak or the time from one peak to another
described as positive (P, below the baseline) or negative (N, above the baseline)
A waveform is identified by the letter describing its deflection above or below the baseline followed by a number indicating its latency (e.g., N20)
INTRAOPERATIVE SSEP's, INDICATIVE OF SURGICAL TRESSPASS / ISCHEMIA INCLUDE,
a . increased latency
b . decreased amplitude
c . complete loss
Any decrease in amplitude greater than 50% or increase in latency greater than 10% may indicate a disruption of the sensory nerve pathways. The spinal cord can tolerate ischemia for about 20 minutes before SSEPs are lost.
ANESTHETIC DRUGS AND SSEP
All of the halogenated inhaled anesthetics probably cause roughly equivalent dose-dependent decreases in amplitude and increases in latency that are further worsened by the addition of 60% nitrous oxide. It is best to restrict the use of volatile anesthetics and nitrous oxide to levels below 1 minimum alveolar concentration (MAC) and not to combine the two. n If possible, bolus injections of drugs should be avoided, especially during critical stages of the surgery. Continuous infusions are preferable.
CONDITIONS ALTERING SSEP
#Hypothermia : increases latency, whereas amplitude is either decreased or unchanged. For each decrease of 1 degree C, latency is increased by 1ms.
#Hyperthermia (4 degree C) : decreases amplitude to 15% of the normothermic value.
#Hypotension: With a decrease of the mean arterial blood pressure (MAP < 40mm Hg), progressive decreases in amplitude are seen. The same change is also seen with a rapid decline in MAP to levels within the limits of cerebral autoregulation.
#Hypoxia: ?Decreased amplitude
#Hypocarbia: Increased latency has been described at an end-tidal CO 2 < 25mm Hg.
#Isovolumic hemodilution: Latency is not increased until the hematocrit is < 15%, and amplitude is not decreased until the hematocrit is < 7%. This effect is likely caused by tissue hypoxia.
#scoliosis surgery & Harrington rod placement
#spinal cord decompression and stabilisation after acute SCI spinal fusion
#brachial plexus exploration following acute injury
resection of spinal cord tumours, cysts & vascular anomalies
correction of cervical spondylosis
#resection of 4 th ventricular cysts
release of tethered spinal cord
#resection of acoustic neuroma
resection of intracranial lesions involving the sensory cortex
resection of thalamic tumours
abdominal and thoracic aneurysm repair
IF SSEP CHANGES SIGNIFICANTLY, WHAT THE SURGEON AND ANAESTHESIOLOGIST CAN DO TO DECREASE THE INSULT?
The anesthesiologist can:
>Increase mean arterial blood pressure, especially if induced hypotension is used.
>Correct anemia, if present.
>Correct hypovolemia, if present.
>Improve oxygen tension.
>Correct hypothermia, if present.
The surgeon can:
>Reduce excessive retractor pressure.
>Reduce surgical dissection in the affected area.
>Decrease Harrington rod distraction, if indicated.
>Check positioning of associated instrumentation (e.g., screws, hooks).
If changes in the SSEPs persist despite corrective measures, a wake-up test may be performed to confirm or refute the SSEP findings. The patient’s anesthetic level is lightened, and a clinical assessment of neurologic function is performed. The monitoring of motor-evoked potentials along with SSEPs provides a more complete assessment of neural pathway integrity. As the sensory pathways are supplied predominantly from the posterior spinal artery & the motor tracts from the anterior, a significant motor deficit can develop without significant change in SSEP's.
Tuesday, November 24, 2015
Severe pain ( > 4 on a 0–10 scale) is commonly experienced during the first 48h with an incidence of nearly 70% on the first postoperative day and 48% on the second postoperative day
Women, younger patients and patients who required opioid analgesics preoperatively report significantly greater levels of postoperative pain
Infratentorial procedures are associated with more severe pain than supratentorial procedures
Reduced pain has been reported with a translabyrinthine as opposed to a suboccipital approach for acoustic neuroma resection
The amount of muscle damage from resection of the temporalis and posterior cervical muscles may also influence the degree of postoperative pain
Preoperative Gabapentin, parecoxib and lornoxicam may reduce opiate-induced hyperalgesia
the addition of ondansetron to PCA has not been shown to reduce nausea and vomiting after craniotomy
evidence suggests that NSAIDs should be stopped prior to neurosurgery and avoided in patients with cardiovascular disease.
Gabapentin given 7 days prior to surgery results in significantly lower postoperative pain scores and morphine consumption during the first 48 postoperative hours compared to phenytoin
Preoperative use of nerve blocks or local anesthetic infiltration reduces intraoperative analgesic requirements and may help to reduce pain in the early postoperative period
#craniotomy , #painmanagement, #painaftercraniotomy , #analgesia , #anesthesia ,#neurosurgery
(Ref: Acute and chronic pain following craniotomy Alana M. Flexman, Julie L. Ng and Adrian W. Gelb, Current Opinion in Anaesthesiology 2010, 23:551–557)
Saturday, November 21, 2015
✍Clinical euvolemia, hypotonic plasma, and less than maximally dilute urine are the clues
✍establish normovolemia by physical examination.
(Patients with SIADH are usually said to have normal volume status. However, they actually have excessive TBW. Unlike excessive saline, which is limited to ECF, excessive water distributes two thirds to the ICF and one third to the ECF. Thus the ECF excess is minor and not usually perceptible by clinical examination. Nonetheless, patients with SIADH have mildly increased ECV, which is sensed by the kidney. The kidney increases GFR, which causes a low uric acid, BUN, and creatinine. The increased ECV also increases ANP and, along with increased GFR, promotes natriuresis.)
✍measure P osm ,U osm ,P Na ,U Na , and U K .
✍exclude pituitary, adrenal, and thyroid dysfunction
✍Confirmatory criteria of SIADH include low P Na ( < 135 mEq/L), low P osm ( < 280mOsm/kg), U osm greater than 100mOsm/kg, U Na greater than 40mEq/L, and [U Na + U K ] greater than P Na .
#SIADH , #anesthesia
Friday, November 20, 2015
✔️Dantrolene inhibits calcium release via RyR1 antagonism and impairs calcium-dependent muscle contraction.
✔️This rapidly halts the increases in metabolism and secondarily results in a return to normal levels of catecholamines and potassium.
✔️Dose is 2 mg/kg; repeat every 5 minutes until vital signs normalise , to a total dosage of 10 mg/kg if needed.
✔️dantrolene takes ~ 6 minutes to have any effect
✔️The solution is prepared by mixing 20 mg of dantrolene with 3 g of mannitol in 60 ml of sterile water.
✔️Since dantrolene is relatively insoluble, preparation is tedious and time consuming, and its preparation should not be the responsibility of the primary anesthesiologist involved in the patient’s management. (May occupy several nurses)
✔️All patients who develop MH, require at least 24 hours of posttreatment management in a critical-care setting as there is chance of reappearance of symptoms ( known as recrudescence )
In the ICU, continue @1mg/kg q6h for 24 hours
may be given enterally if GIT functioning (price ~ 1000 x less)
✔️the actions of dantrolene include:
release of Ca ++ from the SR, without affecting re-uptake
? antagonises the effects of Ca ++ at the actin/myosin - troponin/tropomyosin level
muscular weakness, which may potentiate NMJ blockade ~ 5-15 mg/kg produces significant muscular relaxation
there is no effect on NMJ transmission
up to 15 mg/kg there is no significant effect on the CVS
up to 30 mg/kg there is no significant effect on respiration
#dantrolene , #MalignantHyperthermia, #mh ,#anaesthesia
Thursday, November 19, 2015
THE RIGHT WAY OF ADMINISTERING BLOOD PRODUCTS [ from "THE CLINICAL USE OF BLOOD: HAND BOOK , World Health Organization & Blood Transfusion Safety , GENEVA ]
✔️Prefer a larger cannula: A doubling of the diameter of the cannula increases the flow rate of most fluids by a factor of 16.
✔️In case of Whole blood, red cells, plasma and cryoprecipitate
>Use a new, sterile blood administration set containing an integral 170–200 micron filter
>Change the set at least 12-hourly during blood component infusion
>In a very warm climate, change the set more frequently and usually after every four units of blood, if given within a 12-hour period
✔In case of Platelet concentrates
>Use a fresh blood administration set or platelet transfusion set, primed with saline.
>There is no evidence that warming blood is beneficial to the patient when infusion is slow.
>At infusion rates greater than 100 ml/minute, cold blood may be a contributing factor in cardiac arrest. However, keeping the patient warm is probably more important than warming the infused blood.
>Warmed blood is most commonly required in:
Large volume rapid transfusions:
-Adults: greater than 50 ml/kg/hour -Children: greater than 15 ml/kg/hour
Exchange transfusion in infants
Patients with clinically significant cold agglutinins.
>Blood SHOULD ONLY BE WARMED in a blood warmer. Blood warmers should have a visible thermometer and an audible warning alarm and should be properly maintained.
>Blood should never be warmed in a bowl of hot water as this could lead to haemolysis of the red cells which could be life-threatening.
✔️Severe reactions most commonly present during the first 15 minutes of a transfusion. All patients and, in particular, unconscious patients should be monitored during this period and for the first 15 minutes of each subsequent unit.
✔️The transfusion of each unit of the blood or blood component should be completed within four hours of the pack being punctured. If a unit is not completed within four hours, discontinue its use and dispose of the remainder through the clinical waste system.
Tuesday, November 17, 2015
ADMINISTRATION ROUTES: IV, IM, SC, Intranasal DDAVP/Desmopressin
1. Treatment of central diabetes insipidus 2. Prevention and control of bleeding (primarily when there are thought to be platelet function defects especially uraemia, clopidogrel or cardiopulmonary bypass -related)
PRESENTATION AND ADMINISTRATION:
IV: Minirin 4mcg/ml injection Octostim 15mcg/ml injection Doses of 4mcg or less should be administered undiluted by direct IV injection. For small doses (eg 0.4mcg), 4mcg can be diluted in 10 ml of normal saline. For doses of greater than 4mcg in adults or children weighing more than 10kg, dilute with 50ml of normal saline and infuse the first 5ml slowly over 5 minutes. For children weighing less than 10kg, dilute in 10ml of normal saline and infuse the first 1-2ml over 5 minutes. If no marked tachycardia or other adverse effects are observed, give the remainder slowly over 15 minutes PO: Minirin 0.1mg tablets (white)
Nasal Spray: Desmopressin spray (10mcg/dose), Minirin spray (10mcg/dose), Octostim (150mcg/ dose)
IV: Central diabetes insipidus: 0.4mcg repeated as required (may increase the dose if there is an adequate response)
Prevention and control of bleeding: 0.3mcg/kg (max 24mcg) over 30 minutes (once only) Note: although IM and SC routes can be used, IV is generally the preferred route. PO: 0.1mg -1.2mg daily depending on indication (rarely used by this route in ICU)
Nasal Spray: Not generally administered by this route in ICU
No adjustments needed in CRF
CLINICAL PHARMACOLOGY: Desmopressin is a synthetic analogue of the natural pituitary hormone arginine vasopressin (ADH), an antidiuretic hormone affecting renal water conservation..
1. Hypersensitivity to desmopressin 2. Hyponatraemia
When desmopressin acetate injection is administered to patients who do not have need of antidiuretic hormone for its antidiuretic effect, in particular in paediatric and geriatric patients, fluid intake should be adjusted downward to decrease the potential occurrence of water intoxication and hyponatraemia.
Particular attention should be paid to the possibility of the rare occurrence of an extreme decrease in plasma osmolality that may result in seizures which could lead to coma.
Laboratory tests for monitoring the patient include urine volume and osmolality. In some cases, plasma osmolality may be required.
NB: may cause minor increases in blood pressure requiring changes in levels of vasopressor support.
transient headache, ischaemic stroke, changes in blood pressure causing either a slight elevation or a transient fall and a compensatory increase in heart rate, myocardial infarction, nausea, abdominal cramps, water intoxication and hyponatraemia,Local irritation at site of injection, thrombotic events
Monday, November 16, 2015
# Preoperative treatment with GnRH analogue to shrink the fibroid
# Surgeon may intraoperatively inject dilute Vasopressin ( 1 IU in 100 mL RL) to reduce bleeding. IV Vasopressin can cause raised BP, myocardial ischemia, arrhythmias etc
# Position: Dorsal lithotomy; steep Trendlenberg to move the bowel out of surgical field
# Surgical time :1-4 hours; EBL: 100-600 mL
Puncture of major vessel/ severe bleeding
Insufflation in the wrong place
Need for conversion to laparotomy
Peroneal nerve damage from positioning
# Pain score : 4-6
#laparoscopy,#laparoscopyanaesthesia,#myomectomy, #anaesthesia, #anaesthetist