Anaesthetic Considerations with Hyperparathyroidism by Dr. Arpit.pptx

Anaesthetic Considerations with Hyperparathyroidism, Anatomy, Pathophysiology, History taking, ECG Changes

1. Anesthetic Considerations in Hyperparathyroidism Presentor : Dr. Arpit Patel Moderator: Dr. Bindu K.

2. Anatomy of Parathyroid Glands Parathyroids are the endocrine glands usually located on the posterior aspect of the thyroid gland - within the pretracheal fascia. They are flattened and oval in shape measures 6 × 4 × 2 mm and weighs 40 mg to 60 mg Most individuals have  four  parathyroid glands, although variation in number (from two to six) is common (13%) 16% - present in an ectopic location including the mediastinum or retro-esophageal area 3

3. Superior parathyroid glands located near the posterolateral aspect of the superior pole of the thyroid, 1cm above the junction of the recurrent laryngeal nerve (RLN), and the inferior thyroid artery. They lie deep to the plane of the recurrent laryngeal nerve . Inferior parathyroid glands located near the inferior poles of the thyroid glands They classically lie superficial to the plane of the RLN 3 Superior Parathyroid Inferior Parathyroid

4. Blood Supply & Nerve Relations Arterial supply is mainly by - inferior thyroid artery   Collateral arterial supply is from the superior thyroid artery and thyroid ima artery. Venous drainage is into the  superior ,  middle , and  inferior thyroid veins . The lymphatic drainage from the parathyroid glands is to the  paratracheal  and  deep cervical nodes . The parathyroid glands have an extensive supply of sympathetic nerves derived from  thyroid branches  of the cervical ganglia. 4

5. Structure & Function The parathyroid glands have two distinct types of cells: the chief cells and the oxyphil cells. Chief cells:   The chief cells manage the secretion of parathyroid hormone (PTH). Oxyphil cells:  The purpose of these cells is not entirely understood. They are larger than the chief cells and seem to increase in number with age.  4

6. Calcium Regulation Chief function – Regulation of calcium levels in the blood ↓ in serum calcium  calcium-sensing receptor ( CaSR ) on parathyroid chief cells detects extracellular Ca²⁺  releases - parathormone or parathyroid hormone (PTH). PTH affects target organs - kidneys, intestine, and the skeletal system.   5

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8. Kidney PTH promotes calcium reabsorption and excretion of phosphate. The reabsorption is promoted at the ascending loop of Henle , distal tubule, and the collecting tubules. PTH also promotes 25-hydroxyvitamin D conversion to its active form (1,25-dihydroxy vitamin D-3) via activation of 1-hydroxylase in the proximal tubules. Intestine Activated vitamin D promotes the absorption of calcium 6

9. PTH Secretion & Regulation Bone Rapid Phase PTH affects both osteoblastic and osteoclastic cells. When PTH binds to the cellular receptors, it allows the pumping of calcium from the osteocytic membrane.  This causes an immediate effect and allows for the rise of serum calcium to occur within minutes.  Slow Phase The slow phase takes several days to precipitate an increase in blood serum calcium. This process occurs via the osteoblast 6

10. PTH - Regulation 6 Stimulus Mechanism ↓ Serum Ca²⁺ Removes calcium-sensing receptor ( CaSR ) mediated inhibition ↑ Serum phosphate Binds calcium → ↓ ionized Ca²⁺; possible direct effect ↓ Mg²⁺ Similar effect as low Ca²⁺ β- adrenergic input cAMP-mediated stimulation Low calcitriol Reduced negative feedback on PTH gene expression

11. Why Parathyroid is important in Anesthesia ? The parathyroid glands matter in anesthesia because their dysfunction can profoundly affect calcium balance , which in turn influences Airway safety Cardiac rhythm Muscle relaxant effects Perioperative metabolic stability . 6

12. Parathyroid Abnormalities 6

13. Hyperparathyroidism Definition Hyperparathyroidism is a disorder characterized by excess secretion of parathyroid hormone (PTH) from one or more of the parathyroid glands, leading to disturbances in calcium, phosphate, and bone metabolism. 6 Condition PTH Level Normal 10-65 pg /mL Hypo parathyroid < 10 pg /mL Hyper parathyroid > 65 pg /mL

14. Classification of Hyperparathyroidism Hyperparathyroidism is classified based on the underlying cause of parathyroid overactivity : Primary Hyperparathyroidism This is due to an intrinsic problem with the parathyroid glands themselves. Cause: Autonomous overproduction of PTH (most commonly due to a parathyroid adenoma (≈80% of cases) , less often hyperplasia or carcinoma). Effect: Hypercalcemia , low phosphate. 6

15. Classification of Hyperparathyroidism High calcium can cause the classic clinical manifestations summarized as “stones, bones, abdominal moans, and psychic groans”: kidney stones and nephrocalcinosis , bone pain and osteoporosis, gastrointestinal upset (nausea, constipation, peptic ulcers, pancreatitis), and neuropsychiatric disturbances (fatigue, depression, confusion). 6

16. Classification of Hyperparathyroidism Secondary Hyperparathyroidism Cause: This occurs when an external stimulus (usually chronic hypocalcemia ) causes compensatory parathyroid overactivity . The most common trigger is chronic kidney disease (CKD). In CKD, phosphate retention and reduced renal vitamin D activation lead to hypocalcemia , which persistently stimulates PTH release. Vitamin D deficiency or malabsorption can also cause secondary hyperparathyroidism. 6

17. Classification of Hyperparathyroidism Tertiary Hyperparathyroidism This develops when longstanding secondary hyperparathyroidism causes the parathyroid glands to become autonomously overactive , even after correction of the underlying cause (such as after a kidney transplant). Tertiary hyperparathyroidism results in autonomous PTH secretion and often hypercalcemia (similar to primary hyperparathyroidism, but arising from an evolved secondary process). 6

18. Anesthetic Considerations

19. 1. Pre-operative Evaluation : History taking Detailed History Symptoms of hypocalcaemia General: Fatigue, muscle weakness, psychiatric symptoms (“psychic groans”). Renal: Recurrent renal stones, polyuria, polydipsia, dehydration, chronic kidney disease symptoms. Skeletal: Bone pain, fragility fractures, height loss, difficulty walking. 7

20. Gastrointestinal: Constipation, nausea, vomiting, or abdominal pain (“abdominal moans”) Neurological: Confusion, depression, lethargy, decreased memory. Cardiac: Palpitations, chest pain, syncope, history of arrhythmias or hypertension. 8

21. Past History Medical conditions: Hypertension, ischemic heart disease, chronic kidney disease, diabetes, peptic ulcer disease, pancreatitis, thyroid disorders. Surgical history: Fracture or bone surgery history (due to osteoporosis). History of MEN syndrome (pituitary tumors , pheochromocytoma ). Previous surgeries: neck surgery, parathyroidectomy , renal procedures. 7

22. Previous Anaesthesia History Previous anaesthetic exposure, Complications: Difficult airway, Delayed recovery, Malignant hyperthermia Arrhythmias 7

23. Family & Personal History Family history of MEN syndromes. Alcohol use (worsens bone disease), smoking. Occupation (repeated fractures, bone weakness may affect daily life). Drug & Allergy History Drugs for hypercalcemia : calcitonin, bisphosphonates. Diuretics (esp. thiazides → ↑ Ca ), lithium use. Drug allergies. 7

24. 2. Physical Examination General Examination General appearance – fatigue, lethargy, body habitus. Signs of dehydration – dry tongue, poor skin turgor (due to polyuria). Vital signs – BP (hypertension common), HR ( tachy /arrhythmias), Temperature, RR. Mental status – confusion, depression, altered sensorium (due to hypercalcemia ). Nutritional status – muscle wasting. 9

25. Parathyroid Carcinoma 2. Airway Examination Look for neck swellings / scars (previous thyroid or parathyroid surgery). Airway difficulty if large goiter or MEN syndrome–associated thyroid mass present. Mouth opening, Mallampati grade, neck mobility. 10

26. 3. Lab - Investigations Parathyroid hormone (PTH) levels: elevated (key diagnostic). Ionized calcium : Most accurate for physiological relevance. Total serum calcium (adjust for albumin if ionized calcium not available). Phosphate : T ypically low in primary hyperparathyroidism due to PTH phosphaturia , but high in renal failure cases (Normal = 2.5–4.5 mg/ dL ) Renal function tests : H ypercalcemia can impair renal function and secondary hyperparathyroidism is related to CKD. Vitamin D levels – often deficient especially in secondary causes . 11

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28. 12 Feature Ionized Calcium Total Serum Calcium Definition Free, biologically active calcium in plasma All calcium in plasma (ionized + bound to albumin + complexed) Normal Range 4.5–5.6 mg/dL (1.12–1.32 mmol/L) 8.5–10.5 mg/dL (2.12–2.62 mmol/L) Affected by Albumin Levels No Yes (low albumin → low total calcium even if ionized is normal) Best Use Critical illness, acid–base disorders, hypoalbuminemia, rapid decision-making Routine screening, general labs, long-term monitoring Limitations More expensive, less available May mislead if albumin or pH is abnormal Regulator of PTH Direct regulator No direct effect

29. ECG - Changes Shortening of the QT interval is the hallmark of hypercalcemia . This is primarily due to a shortened ST segment (rapid ventricular repolarization in high calcium states). The P-R and QRS intervals are usually normal, though extremely high calcium levels can cause slight P-R prolongation or QRS widening in some cases. In severe hypercalcemia , one may see Osborn waves (J waves) – a dome-like deflection at the J point (end of QRS) 14

30. 15 ECG Feature Hypocalcemia Hypercalcemia QT Interval Prolonged (mainly due to ST segment prolongation) Shortened (mainly due to ST segment shortening) ST Segment Prolonged Shortened or absent T Wave May be normal or inverted May be flattened or inverted QRS Complex Usually normal Usually normal; severe cases may cause widening Other Features Possible ventricular arrhythmias (Torsades de pointes in severe cases) Possible Osborn (J) waves in severe hypercalcemia ; rare ventricular arrhythmias Mechanism Low Ca²⁺ → delayed ventricular repolarization High Ca²⁺ → accelerated ventricular repolarization

31. 4. Pre-op Optimization Aggressive Hydration: Begin IV fluids (0.9% normal saline) to expand intravascular volume and enhance renal calcium excretion. Hypercalcemia often causes polyuria and dehydration, so most patients arrive volume-depleted. Forced Diuresis: Once the patient is well hydrated, add a loop diuretic such as furosemide to further increase calcium excretion by the kidneys. Loop diuretics inhibit calcium reabsorption in the ascending loop of Henle . Caution: avoid diuretics until volume repletion is achieved (to prevent worsening dehydration). Correct Electrolyte Imbalances: Normalize phosphate levels prior to surgery. Primary hyperparathyroidism often causes hypophosphatemia. In secondary hyperpara , hyperphosphatemia is common due to renal failure; efforts should be made to lower phosphate (dietary restriction or binders) before surgery. 16

32. Medications to Lower Calcium: IV Bisphosphonates (e.g. zoledronic acid or pamidronate ) help drive calcium into bone by inhibiting osteoclasts. Bisphosphonates take 1–2 days to maximal effect, but are very useful in stabilizing calcium preoperatively Calcitonin (salmon calcitonin by subcutaneous or IM injection) acts quickly (within hours) to lower calcium by inhibiting bone resorption and increasing renal calcium excretion. Vitamin D Repletion: If the patient is vitamin D deficient (quite common in secondary hyperparathyroidism and even in many primary cases), start vitamin D supplementation ( ergocalciferol or cholecalciferol ). In renal failure patients, active vitamin D analogs (like calcitriol or alphacalcidol ) are used to help suppress PTH. 17

33. Intra-operative Management Goals Maintain normocalcemia and normophosphatemia . Prevent arrhythmias and hemodynamic instability . Optimize neuromuscular blockade without prolonged recovery. 18

34. Intra-op - Monitoring Standard Monitoring: Apply standard ASA monitors (ECG, noninvasive blood pressure, pulse oximetry , capnography , temperature). Continuous ECG is crucial to watch for arrhythmias (like bradycardia or ventricular ectopics ) that hypercalcemia might precipitate. Invasive arterial line : Consider in major surgery or unstable cases for real-time BP and ABG (ionized calcium) monitoring. 19

35. Gastrointestinal Manifestations Nerve Integrity Monitoring: For parathyroid (and thyroid) surgeries, the surgical team often requests a recurrent laryngeal nerve (RLN) monitoring endotracheal tube. This is a specialized endotracheal tube (NIM tube) with electrodes that contact the vocal cords. It allows intraoperative monitoring of RLN function – if the nerve is stimulated or stretched, the EMG activity is detected. Avoid long-acting muscle relaxants when using nerve monitoring, because a paralyzed vocal cord can’t generate EMG signals. 20

36. Airway Management: Anticipate any airway difficulty. A video laryngoscope is often utilized for intubation to get an excellent view without excessive manipulation (helpful if anatomy is distorted or patient has short neck). Preparation : Ensure airway is ready before deep sedation. pre-oxygenate thoroughly and have calcium ready. Have succinylcholine available for rapid relief if severe. CPAP or gentle positive pressure may abort mild spasm. Special note : In post-thyroidectomy hypoparathyroidism , watch for RLN palsy — may complicate airway. 21

37. Induction and Hemodynamic Management: Induction agents should be titrated carefully. Choose an induction strategy that maintains stability – e.g. etomidate , and have vasopressors ready. Ketamine is generally avoided if the patient is severely hypertensive or has altered mental status (though mild doses could help in an opioid-sparing technique if needed for analgesia). 22 Anesthetic drug – considerations in Hypocalcemia

38. Anesthetic Drugs and Muscle Relaxants: Volatile inhalation agents, IV anesthetics , and opioids can be used as usual, but consider that hypercalcemia may cause resistance to neuromuscular blocking drugs (since high calcium enhances neuromuscular transmission). Thus, if using any paralytic, monitor neuromuscular function (train-of-four monitoring) to guide dosing. Choose short-acting agents that won’t accumulate – e.g. remifentanil infusion for analgesia, and a low dose sevoflurane or desflurane to allow quick wakeup for neurologic evaluation (especially if there’s concern of vocal cord function, you’d want them awake to assess voice). 23

39. Intraoperative PTH Monitoring: Many centers perform rapid intraoperative PTH assays during parathyroid surgery. About 10–15 minutes after the surgeon excises the suspected abnormal gland, a blood sample is drawn to check PTH level drop. A significant fall (e.g. >50% drop from baseline PTH) usually indicates successful removal of hypersecreting tissue. The anesthesiologist coordinates these blood draws (often from the arterial line if present) and communicates results. This helps determine if additional exploration is needed during the same surgery. 24

40. Fluid and Electrolyte Management: Continue IV fluids (usually saline) during surgery to keep up the diuresis that was started pre-op. Monitor urine output. Avoid lactated Ringer’s if calcium is very high, since LR contains calcium; however, a small amount of calcium in LR is usually not clinically significant so it’s not absolutely contraindicated, but many prefer saline in hypercalcemic patients. Check blood glucose if the patient received large volumes of saline (to catch hyperchloremic metabolic acidosis or hyperglycemia in diabetic patients under stress). 25

41. Post- operative Management 26

42. 1. Airway & respiratory monitoring Recurrent Laryngeal Nerve (RLN) Injury: The RLN runs near the thyroid and parathyroid glands and is at risk of stretch or inadvertent damage during surgery. Unilateral RLN injury will cause hoarseness and a weak, breathy voice. Bilateral RLN palsy is rare but serious – it can lead to airway obstruction because both vocal cords become paralyzed in a near-closed position (causing stridor and respiratory distress). In the immediate postoperative period, assess the patient’s voice as soon as they are awake – ask them to speak or say “e” or “moon” (to evaluate vocal cord function). . If there are stridor or signs of obstruction, emergent evaluation is needed – this may include re-intubation or urgent tracheostomy if bilateral vocal cord paralysis is confirmed. 27

43. Neck Hematoma: Though parathyroidectomy is a small incision surgery, any neck surgery carries risk of bleeding into the confined neck space. A neck hematoma can be life-threatening due to tracheal compression. Signs include: neck swelling, a feeling of fullness or choking, neck pain or pressure, difficulty swallowing, respiratory distress, stridor, or neck vein distension 28

44. This typically would occur within the first 6–8 hours after surgery. Immediate action is required if a significant hematoma is suspected: the surgical wound sutures should be released at bedside to decompress the hematoma. The patient may require a return to the OR for evacuation of the hematoma and bleeding control. The anesthesia and nursing teams in PACU must be vigilant – if the patient’s neck dressings feel tight or they complain of difficulty breathing, investigate immediately. Keep basic airway management tools and even fiberoptic scope ready in case intubation becomes necessary due to swelling. 29

45. 2. Cardiac Monitoring Observe QT interval on ECG – prolonged QT can indicate hypocalcemia and predispose to arrhythmias. If the patient exhibits symptoms or if ionized calcium is low, initiate treatment promptly. IV calcium gluconate (or calcium chloride in a central line) is given for symptomatic or significant hypocalcemia . Typically, 1–2 grams of calcium gluconate is infused slowly and repeated as needed, followed by oral calcium and vitamin D supplementation for ongoing management. Monitor serum calcium levels every 6–8 hours initially (or as per institutional protocol). 30

46. 3. Electrolyte Monitoring Postoperative Hypocalcemia : A drop in calcium is common after removal of overactive parathyroid tissue. The remaining normal parathyroids may be suppressed (hungry bone syndrome and “stunned” glands) leading to transient hypocalcemia . Clinical signs to monitor for include: Tetany ( peri -oral or fingertip tingling, muscle cramps, carpopedal spasm), Chvostek’s sign (facial muscle twitch with tapping the facial nerve), Trousseau’s sign (carpal spasm with a blood pressure cuff), and In severe cases laryngospasm or seizures. 31

47. Two Important Tests 1. Chvostek sign Twitching of the upper lip, cheek with tapping on the cheek 2 cm anterior to the tragus , in the facial nerve distribution area

48. 2. Trousseau sign more reliable sign present in 94% of hypocalcemic pts carpopedal spasm - following application of an inflated BP cuff over systolic pressure for 3 min The flexed wrist and metacarpophalangeal joint, and the extended fingers are characteristic of Trousseau sign

49. 4. Pain & ventilation management Parathyroid surgery pain is usually moderate and mostly focused in the incision area of the neck. Multimodal analgesia is effective: use acetaminophen and NSAIDs (if not contraindicated) to reduce opioid requirements. An opioid like morphine or hydromorphone in small doses can be given for breakthrough pain, but avoid oversedation . Local anesthetic infiltration or regional blocks (like a superficial cervical plexus block) done by the surgeon can dramatically reduce pain and opioid need. 32

50. Take Home Message Hyperparathyroidism results in systemic hypercalcaemia with multi‑organ effects Pre‑operative optimisation requires aggressive hydration, diuresis and correction of electrolytes Intra‑operative management emphasises nerve integrity monitoring and careful airway control Post‑operative vigilance for hypocalcaemia, haematoma and RLN injury is essential 32

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