CARCINOID SYNDROME & THE ANESTHESIOLOGIST

🌋Carcinoid tumours are neuroendocrine tumours originating from enterochromaffin cells [GIT(~90%), gonads and bronchus mainly]

🌋 Some patients develop Carcinoid Syndrome, where the tumour secretes neuropeptides into systemic circulation 

🌋 Usually they undergo firstpass metabolism in liver

🌋 If the patient is becoming symptomatic, due to the neuropeptide secretion, it's either due to their production in large amounts to overwhelm the metabolic capacity of the liver or that they are released without going through the portal circulation 

🌋 They secrete bio-active compounds like serotonin, histamine, catecholamines, bradykinin, kallikrein, substance-P, motilin etc

🌋 This can cause symptoms like bronchospasm, hypotension, hypertension, flushing etc

🌋 Pharmacologic treatment of intraoperative/ acute/ hemodynamic crises are with i.v. Octreotide, whereas for treatment of chronic symptoms, Somatostatin analogues like Lanreotide are used. Octreotide can also be used for prophylaxis. Should be continued postoperatively.

🌋 Vasoactive drugs like catecholamines and histamine releasing drugs like morphine, atracurium, succinylcholine, thiopentone etc should be avoided. Use of a test dose may reduce adverse events. 

🌋 Antihistamines are also given prophylactically in case of gastric tumours

🌋 Another concern for the anesthesiologist in such patients is the possibility of Carcinoid heart disease.  Here, the patient develops thickened valves resulting in tricuspid and pulmonary regurgitation and pulmonary stenosis (mitral and aortic insufficiency can also occur,; but are less frequent). Pericarditis or myocardial metastases can also occur.

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WHY RELATIVES SHOULD BE AN INTEGRAL PART OF THE CHAIN OF HEALTHCARE ❓

PEAK EXPIRATORY FLOW RATE

😤 It's the maximal rate of airflow during forced expiration 

😤 Dependent on patient-effort

😤 Repeated 3 times and the best of the 3 is taken

😤 Trends in Peak Expiratory Flow helps to assess the severity status of an acute episode, response to treatment etc

😤 Normal values: Females: 250-500 L/min Males:450-700 L/min

😤 METHODS TO MEASURE:

🎚 Wright’s Peak flow meter : Commonly used clinically and is a constant pressure variable orifice device

🎚 Pneumotachograph : Used for research purposes and is a variable pressure constant orifice device

🎚 From flow volume loops : They are plots of airflow at various lung volumes. Help to distinguish between obstructive & restrictive devices

What will happen if we give a large Carbohydrate diet to an already malnourished patient in the ICU❓

🔰If we introduce nutritional support ( enteral or parenteral)  based on the requirements of  a regular healthy adult, to a malnourished patient, there will be a significant rise in basal insulin secretion, which will draw Potassium and Phosphate into the cell leading to hypokalemia, hypophosphatemia and fatal fluid shifts. ( Both rapid initiation and large amounts are dangerous). Phosphate depletion is also associated with increased urinary Magnesium excretion.

🔰 It can also be associated with Renal failure, Respiratory failure, Neuromuscular failure, Cardiac failure and Arrhythmias

🔰 This is known as “Refeeding Syndrome“

🔰 So to avoid this, in patients at risk ( e.g. chronic alcoholics, those who have not eaten anything in last 5 days etc) , we should introduce nutritional support at not more than 50% of the daily requirement , for the first two days.

🔰 Feeding rates can be increased to normal levels, if there is no evidence of refeeding syndrome clinically and biochemically, thereafter.

🔰 NICE guidelines for the high risk patients : start support with a maximum 10 kCal per kg per day, with thiamine & B complex supplementation. Biochemical parameters to be monitored closely.

🔰 There is no need for Prefeeding correction of  electrolytes 

Reference: Mehanna HM, Moledina J. Refeeding syndrome: What it is, and how to prevent and treat it. BMJ. 2008; 336(7659): 1495–1498.

Iron (Fe) metabolism

We ingest dietary iron in the form of either as free Fe or as haem bound Fe

The efficiency of absorption varies & is between 5-25% only☹️

It also depends on total body  Fe stores

We cannot expel iron by metabolism: then what's the way❓(1) We depend on slow losses through cell sloughing, menstruation, bleeding etc (2) We absorb only what we want

Fe is absorbed through duodenal & jejunal mucosa

If it's free Fe, it attaches itself to a specific receptor ( it's expression depends on the total body Fe stores) on the apical membrane of the cell. Fe is absorbed by active transport.

If haem-bound Fe, it enters the cell by pinocytosis, and inside the cell, haem is broken down 

Here it binds with apoferritin to form ferritin, which is the intracellular storage form. 

When required, Fe is released into the plasma. Here it binds with the transport molecule beta-transferrin ( it's expression is also dependent on total body Fe store)

A FEW FACTS ABOUT THE ADJUSTABLE PRESSURE LIMITING (APL) VALVE [📖]

🔗 When fully opened the APL valve maintains a pressure of around 1.5 cm of H2O 

🔗 As we close the APL valve, the pressure builds up inside and there is a safety overpressure release valve is incorporated in modern APL valves, to avoid this rising to dangerous levels. This system starts opening at  a pressure of 30 cm of H2O and fully opens at 60 cm of H2O and at this point, allows the gases to escape at a rate of 50L/ min 

🔗 When the patient inspires, the APL valve , if intact, should not allow entrainment of air from the environment 

🔗As the modern reservoir bags are less compliant, compared to the older latex ones, the importance of overpressure relief valves has increased

🔗 As the APL valve will always produce a small resistance to expiration, even when maximally loosened, it helps to maintain PEEP

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AMNIOTIC FLUID EMBOLISM (AFE) : WHICH ARE THE CONSISTENT CLINICAL FEATURES @ PRESENTATION❓

🎯 Hypotension , Hypoxemia and DIC are hallmarks (Ⓜ️NEMO> "AFE is Highly Dangerous")

🎯 Hypotension & Fetal Distress occur in 100% of cases

🎯 DIC occur in 83% and indicate a bad prognosis 

🎯 Cardiac arrest occur in around 87% of patients

🎯 Mortality is >60% ; it has been observed that only 15% survive with intact neurological function 

🎯 Pulmonary Hypertension, CHF and DIC are key events in the pathogenesis

🎯 Pulmonary edema (occur in >90% of cases),Dyspnoea (occur in 49%) & Bronchospasm (occur in 15%) are the respiratory signs

Reference: Dedhia JD, Mushambi M. Amniotic fluid embolism. Contin Educ Anaesth Crit Care Pain. 2007; 7(5): 152–156. Gist RS, Stafford IP, Leibowitz AB et al. Amniotic fluid embolism. Anaesth Analg. 108(5): 1599–1602.

EXAMPLES OF 'SMALL' THINGS WHICH CAN SIGNIFICANTLY IMPAIR PATIENT'S SATISFACTION

The Risk Factors as per EuroSCORE II System used for risk stratification of patients undergoing Cardiac Surgery

📊Patient factors 

• Sex: Female 

• Age: >60 years 

• Co-morbidities including renal, neurological and extra-cardiac arterial disease 

📊Disease factors 

• Recent MI 

• Left ventricular dysfunction 

• Unstable angina 

📊Operative factors 

• Redo or emergency surgery 

• Non-isolated coronary artery bypass grafting

EPIDURAL NEEDLE & CATHETER : KNOW THE MEASUREMENTS

📐 The adult needle is 10 cms long ( shaft measures 8 cms ). 15 cms long needles are also available for obese patients 

📐 The markings are 1 cm apart for the adult needle and 0.5 cm for the pediatric one

📐 For the adult 16 & 18 G are the commonly used ones, whereas for the pediatric 19 G needles are available 

📐 Touhy is the commonly used needle

📐 Regarding the tip: ✔️The bevel is angled at 20 degree with the shaft ✔️ It is known as Huber point ✔️ It's blunt ✔️ All these features aid in the effectiveness of Loss of Resistance Technique 

📐 Regarding the catheter: ✔️ It's made of nylon or teflon ✔️ The distal tip is rounded and closed ✔️So fluid can escape only through the side ports. All these features helps to reduce chances of dural puncture and vascular injury

📐 The adult catheter is 90 cms long

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