Q74. Write a note on options of pain management in surgery.
Ans. Pain is a sensory and an emotional experience that is brought about by actual or potential tissue damage or described in terms of tissue damage.
y Acute pain: Pain duration < 1 month and pain that resolves within hours or at the most few days after the wihtdrawl of the stimulus or wound healing.
y Chronic pain: Pain that persists > 1 month beyond the expected time of healing/
recovery.
Types of pain
y Nociceptive pain (muscle or viscera or skin and subcutaneous tissue origin) y Neuropathic pain (nerve origin)
y Psychogenic pain (mental origin).
Pain control methods in chronic painful conditions are as follows:
y Local medications such as anesthetic drugs, topical analgesia, topical steroids y Nerve stimulation procedures such as acupuncture, transcutaneous electrical nerve
stimulation (TENS)
y The pain management step ladder for oral and parenteral analgesics – Simple analgesics: Aspirin and NSAIDs
– Second step analgesics: Tricyclics, Pregabalin – Third step: Mild opioids such as tramadol
– Final stand: morphine—oral, parenteral or epidural—continuous or patient controlled y Management of phantom limb as described in the question on amputation is an example
of pain management for chronic conditions and should be described here as an example.
Pain management of malignant conditions
y This also begins with the analgesic step ladder and proceeds to further neurolytic nonsurgical and surgical techniques
y These include techniques such as celiac ganglion block for pain due to pancreatic cancer, intrathecal neurolysis, anterolateral cordotomy as well as radiation therapy for pain relief (This is described in the question on functional neurosurgery in neurosurgery section) y Other methods of pain relief involve hormones such as steroids and anti-pituitary drugs,
psychotherapy, group therapy, physiotherapy and anticonvulsants can also be used for pain relief in these conditions.
y It is associated with common medical and surgical conditions including sepsis, severe trauma, multiple transfusions, pancreatitis, multiple transfusions, burns and drug overdose.
y Mortality : 26 to 44%. High index of suspicion and early identification is required for adequate management.
y Etiology – Pneumonias – Sepsis – Trauma
– Post cardiopulmonary bypass – Near drowning
– Toxic lung injury y Diagnostic Criteria
– Multiple definitions had been proposed till the one got published in 1994 proposed by AECC (American and European Concensus Conference) based on PaO2/FiO2 ratio, PAWP and Chest Radiograph showing infiltrates.
– Berlin Definition:
- Within 1 week of known clinical insult or worsening respiratiory symptoms - Bilateral opacities – not fully explained by effusions, lobar/lung collapse or nodules - Oxygenation
a. Mild – 200 mm Hg < PaO2/FiO2≤ 300 mm Hg with PEEP or CPAP ≥ 5 cm H20 b. Moderate – 100 mm Hg < PaO2/FiO2≤ 200 mm Hg with PEEP or CPAP ≥ 5 cm
H20
c. Severe – PaO2/FiO2≤ 100 mm Hg with PEEP or CPAP ≥ 5 cm H20
- Origin of edema : Respiratory failure not fully explained by cardiac failure or fluid overload
– ARDS can be multifactorial. Presence of two predisposing conditions can synergistically aggravate ARDS.
– Predisposing factors: Old age, metabolic acidosis, alcohol consumption, decreased immunity.
y Pathophysiology/natural history – Exudative phase
- Encompases first 7 days
- Injury to the cells (Type 1 pneumocytes) > endothelial injury > inflammatory exudation
- Increased cytokines like interleukin 1, TNF > attracts leucocytes > activates leucocytes > further release of pro inflammatory chemokines
- Cellular debris + protein aggregation = hyaline membranes - Endothelial injury of pulmonary vasculature causes microthrombi
– Proliferative phase
- Usually lasts from 7th day to 21st day
- Critical phase of mechanical ventilation ends in this stage
- Tachypnea, dyspnea, hypoxemia still persist due to increased work of breathing - Histologically: Shift from neutrophilic to lymphocytic exudate and initiation of
lung repair
- Proliferation of type 2 pneumocytes – Fibrotic phase
- Most patients recover within 3 to 4 weeks after initial lung injury, some patients enter a protracted course with fibrotic phase.
- Interstitial fibrosis and organization of the exudates ensues.
- Acinar architecture is markedly disorganized.
- Mortality substantial if clinical course prolongs to fibrotic phase.
y Treatment – General care
- Treatment of the underlying cause - Fluid balance
- Minimize procedures and their complications
- Prompt identification of nosocomial infection and antibiotics - Adequate nutrition
– Mechanical ventilation
- Cornerstone of the management of ARDS
- ARDS specifically increase the risk of ventilator induced lung injury (VILI) a. ARDS is a heterogeneous disorder with predisposition to dependent alveoli b. Different areas with different pulmonary compliance are created
c. Mechanical ventilation causes overdistention of the more normal alveoli and hence leads aggravation of lung injury
d. Rhythmic collapse of the alveoli occurs during mechanical ventilation aggravating the lung injury
- Strategies to prevent VILI a. Low tidal volume
» Low tidal volume, 6 mL/kg compared to conventional tidal volume 12 mL/
kg improved survival and extubation rate among ARDS patients b. High PEEP
» High PEEP prevents the collapse of alveoli at end expiration and hence prevents the extra lung injury occurring during the collapse
» Keeping PEEP high (around 12 to 15 cm H2O) prevents VILI and hence prolongs survival as compared to “normal” PEEP of 5 to 8 cm H2O
» Inversion of I : E ratio (inversion to expiration ratio) will prolong inspiration, leaves less time for expiration. Residual air present in the airways during expiration causes auto-PEEP and hence prevents collapse of alveoli.
c. Prone position
» Certain studies improved oxygenation in prone position due to recruitment of the basal alveoli but survival benefit was not obtained in them.
d. Other strategies
» High frequency ventilation (HFV) at 5–20 cycles/second and tidal volume 1–2 mL/kg
» Partial liquid ventilation (PLV) has revealed promising results initially but no survival benefit was seen
» ECMO—extracorporeal membrane oxygenation
» Data in support of the efficacy of “adjunctive” ventilator strategies are incomplete, hence should not be used routinely.
– Central pressure monitoring
- Routine PCWP be monitored in these patients. Low normal PCWP should be maintained to prevent further dip in oxygenation
- Diuretics and fluid restriction should be used in paitents with concomitant cardiac dysfunction
– Glucocorticoids
- Current evidences do not support routine treatment of ARDS with glucocorticoids.
– Functional recovery
- Majority of the patients have normal functional recovery. Few patients with prolonged mechanical ventilation, ongoing pulmonary assault after development of ARDS undermine the functional recovery in a patient of ARDS.
Q76. Write a note on diabetic ketoacidosis and hyperglycemic hyperosmolar state.
Ans.
y DKA and HHS are acute metabolic complications of diabetes mellitus (DM)
y DKA was considered to be a hallmark of type 1 DM but it also occurs in individuals who lack immunologic features of type 1 DM and do not necessarily require insulin for control after the acute complication (DKA/HHS)
y Both of them represent a continuum of hyperglycemia with or without ketosis.
DKA
Clinical features y Symptoms
– Nausea/vomiting – Thirst/polyuria – Abdominal pain – Shortness of breath y Physical findings
– Tachycardia
– Dehydration/hypotension
– Tachypnoea/Kussmaul’s breathing/respiratory distress – Fruity odor (acetone)
– Abdominal tenderness (may resemble acute pancreatitis or surgical abdomen) – Lethargy/obtundation/cerebral edema/possibly coma
y Precipitating event – Inadequate insulin – Administration
– Infection (pneumonia/UTI/gastroenteritis/sepsis) – Infarction (cerebral, coronary, mesenteric, peripheral) – Drugs (cocaine)
– Pregnancy.
Pathophysiology
y Both deficiency of insulin and excess of glucagon are required for the development of DKA. Insulin deficiency promotes glycogenolysis, gluconeogenesis and lipolysis, all of which leads to the formation of acetyl-CoA and subsequently ketone bodies (acetoacetate, beta hydroxybutyrate and acetone)
y Insulin deficiency leads to inhibition of GLUT4 receptor, preventing the uptake of the glucose by the skeletal muscles and fat aggravating hyperglycemia
y Insulin deficiency shifts the balance of fatty acid metabolism from lipogenesis to lipolysis leading to production of large amount of fatty acids
y Normally increased fatty acids are converted into triglycerides in the presence of insulin, but insulin deficiency and hyperglucagonemia results into further degradation of fatty acids to acetyl-CoA, subsequently forming ketone bodies
y DKA is often precipitated physiological strain to the body leading to production of stress steroids, glucagon in a diabetic patient already deficient in insulin. DKA secondary to infections is common. Inadequate administration of insulin, non-compliance are important precipitating causes.
Laboratory tests
y Routinely monitored tests include complete hemogram, glucose, acid base gas analysis, blood urea, serum creatinine, Na, K, Cl, P
y Triad of features: Hyperglycemia, ketosis and metabolic acidosis y Metabolic acidosis
– Due to production of the ketone bodies
– Arterial pH ranges from 6.9 to 7.3 based on the severity of the acidosis
– HCO3– are generally <10 mEq/L. Hypocarbia is a feature of partial respiratory compensation
– Anion gap is high in DKA. It is generally in the range of 20 to 40 mEq/L y Hyperglycemia
– It is usually in the range of 500 mg/dL
– Causes of euglycemic DKA has been described below:
- Obtunded patient with decreased oral intake - Pregnancy
- Partially/poorly treated DKA with only insulin and no IV fluids y Ketosis
– Detected with urinary ketone dipsticks
– It can be false negative in situations with excessive beta hydroxybutyrate (a ketone) which cannot be detected by nitroprusside test generally employed in the dipsticks – Serum beta-hydroxybutyrate levels are required for further diagnosis
y Potassium is actually deficient in the body, however, normal or hyperkalemia are not uncommon in DKA (secondary to acidosis or decreased renal clearance as in AKI) y Sodium is low in measurement as a consequence of the hyperglycemia
– Corrected sodium : measured sodium + 0.016 (glucose–100) y Hypertriglyceridemia is seen in certain patients
y Leucocytosis and hemoconcentration can be present due to underlying infection and severe dehydration
y Serum amylase should be evaluated to differentiate from pancreatitis, a common condition presenting with abdominal pain
y Serum osmolarity = (2 sodium) + (BUN/2.8) + (Glucose/18) – Mildly or moderately increase in DKA (300–320 mOsm/L) – Very high in HHS (330–380 mOsm/L)
Differential diagnosis y Lactic Acidosis
– Decreased tissue oxygen delivery in settings of hypotension, shock and dehydration – Serum lactate > 5 mmol/L normal ketones and normal glucose in pure lactic acidosis – Can be a contributing factor in DKA with sepsis or dehydration.
y Starvation ketosis – Normal blood glucose
– High urinary ketones and normal blood ketones – Arterial pH is normal mildly raised anion gap.
y Alcoholic ketoacidosis
– Normal pH with respiratory alkalosis often present due to delirium tremens, agitation – Blood ketones and urinary ketones invariably raised
– Normal blood glucose or hypoglycemia
– Treated with IV fluids, thiamine and carbohydrates.
y Uremic acidosis
– BUN, S. creatinine are raised – Normoglycemia.
y Toxic ingestions
– Proper history and examination can rule out salicylate and ethylene glycol, common toxic ingestions with high anion gap and metabolic acidosis.
Treatment
After initiating IV fluid replacement and insulin therapy, the agent or event that precipitated the episode of DKA should be sought and aggressively treated. If the patient is vomiting or has altered mental status, a nasogastric tube should be inserted to prevent aspiration y Fluids
– Fluid deficit of the order of 5 to 10 L are common in DKA and even larger in HHS.
- Water deficit in liters: 0.6 Wt. in kgs (sodium/140 – 1) – Initial bolus of 0.9% Saline: 2 to 3 L over 1 to 3 hours
– Meantime, the laboratory investigations are available, further fluid management is based on the calculation of water deficit.
– 0.45% saline: One-half of the total body deficit + urinary loss to be corrected in next 12 hours and remaining over next 24 hours.
– Use of 0.45% saline reduces the incidence of hyperchloremic metabolic acidosis seen due to rapid volume expansion
– When plasma glucose reaches 250 mg/dL: change to 0.45% saline + 5% Dextrose saline to maintain the blood glucose in level of 200 to 250 mg/dL for next 24 hours along with insulin infusion to allow slow equilibrium of osmotically active substances across cell membrane
– Rapid fluid replenishment in hyperosmolar patients can precipitate cerebral edema and should be avoided
y Insulin
– I.V. bolus of 0.1 IU/kg immediately followed by I.V. infusion of 0.1 IU/kg/hr to provide continuous circulating insulin
– Insulin should not be administered if S. Potassium is less than 3.3 mEq/L
– If glucose concentration doesn’t decrease by 50 mg/dL within 1st hr, second bolus of 0.1 IU/kg should be given and infusion rate increased by 50% or 100%
– Insulin rate should be decreased to 0.05 to 0.1 IU/kg/hr
– As soon as the patient becomes orally accepting, long acting insulin + short acting insulin should be administed. Insulin infusion should be stopped after 30 minute of subcutaneous insulin administration to prevent decrease in S. insulin concentration – A brief period of insulin deficit during transition can cause relapse.
y Potassium
– DKA is a condition with potassium deficit. (3 to 5 mEq/kg)
– Potassium should not be administered before laboratory investigations/ECG are available
– When ECG features of hyperkalemia (tall T waves, QRS widening) are absent or S. K+ is <5.5 mEq/L, potassium should be administered at 10 mEq/hr
– When S. K+< 3.5 mEq/L, administer 40 to 80 mEq/hr – Causes of hypokalemia in DKA therapy
- Insulin mediated intracellular shift
- Correction of acidosis causing intracellular shift
- IV fluids causing brisk diuresis with urinary potassium loss y Bicarbonate
– Despite bicarbonate deficit, it need not to be administered. Insulin causes metabolic conversion of ketones to bicarbonate
– No benefit of bicarbonate therapy in clinical studies of DKA patients – Bicarbonate should be administered when
- pH is < 6.9, hemodynamic instability with pH < 7.1 - with hyperkalemia on ECG findings
– Given as : 50 mEq/L in 200 mL sterile water with 10 mEq/L of KCl per hour until pH > 7.0 – Potassium is given to prevent acute drop in K+ which occurs with correction of acidosis.
y Phosphate
– No benefit of phosphate administration.
Monitoring
y Frequent laboratory investigations, fluid input/output charting and vital signs are the cornerstone of the management of DKA. The importance of a comprehensive chart of clinical and laboratory parameters as a function of insulin cannot be underestimated y Bladder catheterization is required if patient cannot void at will
y ICU and continous ECG monitoring are required if pH is less than 7.3
y Baseline: Complete hemogram, BUN, creatinine, electrolytes, glucose, ketones, lactate, urinalysis, ABG, ECG and upright chest radiograph
y Hourly: Glucose and electrolytes till IV insulin is given; then 2–4 hourly y 6 hourly: BUN, creatinine, ketones
y Intensive monitoring is generally required for the first 12 hours.
Goal is to correct DKA with its metabolic complications completely within 36 hours.
Q77. Write a note on adrenal insufficiency and its management.
Ans. Etiology
y Primary (Adrenal): Deficiency of the secretion of the glucocorticoids and mineralocorticoids from the adrenal glands
– Autoimmune adrenalitis
– Autoimmune polyglandular syndrome 1 and 2 (APS1 and APS2) – Congenital adrenal hyperplasia
– X-linked adrenoleukodystrophy – Infections: Tubercular, HIV, CMV
– Infiltrations: Lymphomas, sarcoidosis, amyloidosis, hemochromatosis – Ketoconazole, suramin, trilostane
y Secondary: Inappropriately low stimulus from the pituitary due to low secretion of the ACTH.
– Pituitiary tumors (endrocrinaly active or inactive)
– Intracranial SOLs: Meningioma, craniopharyngioma, ependymoma – Autoimmune hypophysitis
– Sheehan syndrome – Pituitary irradiation
y Teritiary: Hypothalamic signal disruption/suppression to pituitary for the secretion of ACTH.
– Chronic glucocorticoid excess followed by sudden withdrawal (most common).
Clinical Manifestations
y Primary adrenal insufficiency commonly presents with the symptoms and signs of mineralocorticoid as well as glucocorticoid deficiency while secondary adrenal insufficiency presents with just glucocorticoid deficiency with history of prolonged steroid ingestion followed by abrupt stopping of the drug or intracranial lesion
y Adrenal androgen secretion is disrupted in both primary and secondary adrenal insufficiency
y Chronic adrenal sufficiency
– Lethargy, fatigue, loss of energy, anorexia – Myalgia, joint pain
– Pigmentation is the differentiating feature between primary and secondary adrenal insufficiency.
- Primary: Decreased glucocorticoids >> raised ACTH >> raised POMC (Pro opiomelanocortin) >> increased pigmentation
- Secondary: Absent or abnormal ACTH and POMC >> paleness – Hyponatremia
– Hypoglycemia – Hyperkalemia
– Hypotension, postural hypotension
– Fluid loss due to reduced mineralocorticoids can cause AKI y Acute adrenal insufficiency
– Non specific complain of lethargy and weakness – Postural hypotension progressing to hypovolemic shock
– Acute abdomen can be presenting feature of acute adrenal insufficiency – Nausea, vomiting
– Predisposing factors to acute insufficiency in case of primary chronic insufficiency - Infections
- Hyperthyroidism - Surgical stress.
Treatment
y Acute adrenal insufficiency requires immediate fluid therapy and glucocorticoid administration
y Diagnosis should not hamper the early initiation of the treatment. Random S. cortisol level sample should be withdrawn and glucocorticoid (hydrocortisone 100 mg stat f/b 100 to 200 mg/ day in divided doses) should be administered. Cosyntropin test and other definitive diagnostic techniques are to be deferred until a later time
y Mineralocorticoid, are not to be given separately until hydrocortisone dose is > 50 mg/
day because the daily requirement is met by intrinsic activity of hydrocortisone y Glucocorticoid replacement
– Prolonged glucocorticoid administration is the cornerstone of the treatment of acute adrenal insufficiency
– Daily requirement: 15 to 20 mg of hydrocortisone in two –three divided doses – Dose equivalence
1 mg hydrocortisone = 0.25 mg prednisolone = 0.025 mg dexamethasone
– Half of the dose should be administered in the morning. However, present delivery systems and preparations do not mimic the normal physiological secretion of the body
– Long acting preparations like dexamethasone and prednisolone are not preferred because of prolonged stimulation of the glucocorticoid receptor causing disruption of the normal cycling secretion
– Monitoring
- Signs, symptoms, blood pressure and volume status monitoring
- In primary adrenal insufficiency, monitoring of thyroid status for autoimmune thyroiditis
- If daily dose of glucocorticoid > 30 mg/day of hydrocortisone, then a bone marrow density evaluation is required
– Dose modification is required in conditions of stress. Dose should be doubled by the patient in fever, while undergoing operation, vomiting and trauma
y Mineralocorticoid replacement
– Mineralocorticoid supplementation should begun at a dose of 100 to150 µgm/day – Monitoring is done by blood pressure and postural hypotension evaluation – 40 mg of hydrocortisone is equivalent to 100 µgm of fludrocortisone – Dose is doubled, i.e. 200 µgm/day in summers in tropical countries y Adrenal androgen replacement
– It is optional, indicated in patients with lethargy and weakness after optimum dose of glucocorticoid and mineralocorticoid replacement
– 25 to 50 mg of DHEA once a day
– It is also indicated in females with features of adrenal insufficiency.
Q78. Write a note on myxedema coma.
Ans.
y Myxedema coma is defined as severe hypothyroidism leading to decreased mental status, hypothermia and other symptoms related to slowing of functions in multiple organs y It is a medical emergency with a high mortality rate
y Early recognition and therapy of myxedema coma are essential. Treatment should begun on the basis of clinical suspicion without waiting for laboratory results
y A history obtained from family members often reveals antecedent symptoms of thyroid dysfunction followed by progressive lethargy, stupor and coma.
Clinical presentation
y The function of virtually every organ system and the activity of many metabolic pathways are slowed in severe hypothyroidism
y Hallmarks of myxedema coma are:
– Decreased mental status and – Hypothermia
y Hypotension, bradycardia, hyponatremia, hypoglycemia and hypoventilation are often present as well. Puffiness of the hands and face a thickened nose, swollen lips and an enlarged tongue may occur secondary to nonpitting edema with abnormal deposits of mucin in the skin and other tissues (myxedema).
Neurologic manifestations
y Despite the name, myxedema coma patients do not necessarily present in coma, but do manifest lesser degrees of altered consciousness
– May present in the form of confusion with lethargy and obtundation
– More activated presentation may occur with prominent psychotic features, so-called myxedema madness
– Untreated patients will progress to coma
y It has been reported that focal or generalized seizures may occur, sometimes due to concomitant hyponatremia, and status epilepticus.
Hyponatremia
y Hyponatremia is present in approximately one-half of patients with myxedema coma y It can be severe and may contribute to the decrease in mental status. Cause is uninterrupted
excess secretion of ADH (normally under negative inhibition of T4 hormone).
Hypothermia
y Hypothermia is present in many patients with myxedema coma. Temperature as low as 23°C has been seen with myxedema coma. It is due to the decrease in thermogenesis y The severity of hypothermia is related to mortality in severe hypothyroidism.