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MSC - F. Surgery Answers 2025

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2.Pregnancy in 1st trimester (to avoid fetal thyrotoxicosis)

3.Children/adolescents with thyrotoxicosis

4.Complications of DTG: thyrotoxic heart, liver dysfunction, encephalopathy

5.Drug intolerance/toxicity (agranulocytosis, liver damage)

6.Inaccessibility to long-term follow-up or non-compliance

III. Preoperative Preparation

Objective: Achieve euthyroid state to prevent thyroid storm

Steps:

Mercazolil (methimazole) 20–60 mg/day

Propranolol or other β-blockers

Sedatives, anxiolytics

Glucocorticoids in severe cases

Plasmapheresis (optional, in resistant/severe thyrotoxicosis)

Special note: In diabetics, manage blood sugar alongside (insulin control)

In pregnancy, surgery is safest in 2nd trimester, but 1st trimester may be considered if life-threatening

IV. Surgical Technique

Standard: Subtotal (near-total) thyroidectomy

Performed under general anesthesia

Removes majority of thyroid tissue but spares small remnant to avoid lifelong hypothyroidism

Intraoperative frozen section may be used to rule out carcinoma

Post-op:

Continue antithyroid drugs + beta blockers for 2–3 days

Monitor for:

o Thyroid storm

o Recurrent laryngeal nerve injury

oHypocalcemia (parathyroid injury)

Discharge in 5–7 days if stable

Work ability resumes in 3–4 weeks

7.Autoimmune thyroiditis. Etiopathogenesis, clinical picture, diagnosis, treatment.

THYROIDITIS – OVERVIEW

Thyroiditis is inflammation of the thyroid gland. It may be:

Acute (Infective)

Subacute (Granulomatous/De Quervain’s)

Chronic (Autoimmune – e.g., Hashimoto’s, Riedel’s)

Hashimoto’s Thyroiditis (Chronic Lymphocytic / Autoimmune Thyroiditis)

Etiopathogenesis:

Most common thyroiditis, autoimmune in origin

Formation of antibodies against: o Thyroglobulin (TGHA)

o Thyroid peroxidase (TPO / antimicrosomal Ab)

Associated with other autoimmune conditions: RA, Addison’s, DM1,

pernicious anemia

Familial predisposition (HLA-DR5, DR3)

Pathology:

Diffuse symmetrical thyroid enlargement

Lymphocytic infiltration, Askanazy (Hurthle) cells

Gradual fibrosis, nodularity

Clinical Features:

Middle-aged females

Painless goiter, firm or rubbery

Symptoms of hypothyroidism (fatigue, weight gain, cold intolerance, bradycardia)

Early phase may have transient hyperthyroidism (“Hashitoxicosis”)

May co-exist with papillary thyroid carcinoma

Diagnosis:

High TSH, low T3/T4 (hypothyroid)

Positive anti-TPO and anti-Tg antibodies

FNAC shows lymphocytes, Hurthle cells

Ultrasound: hypoechoic, heterogeneous gland

Thyroid scan: low uptake

Treatment:

Euthyroid + small goiter: No treatment

Hypothyroid: Lifelong levothyroxine

Surgery Indications:

1.Large goiter with pressure symptoms

2.Cosmetic concerns

3.Suspicion of malignancy (nodular/rapid growth)

4.Retro-sternal extension

Surgical Approach:

Lobectomy + Isthmectomy or Subtotal thyroidectomy

Post-op: lifelong suppressive levothyroxine

Hashimoto’s = autoimmune, common, painless goiter + hypothyroid → thyroxine

8. Thyrotoxic crisis, damage of the recurrent nerve, bleeding.

Complication Time of Onset Key Sign Emergency Action

Thyrotoxic

24–48h

Hyperpyrexia, AF,

ICU, antithyroid drugs,

crisis

post-op

delirium

steroids, iodine

Hemorrhage

Immediate to

Neck pressure,

Emergency decompression &

24h

stridor

OR

RLN injury Immediate Hoarseness, stridor Tracheostomy if bilateral

1. THYROTOXIC CRISIS (Thyroid Storm)

Definition:

A life-threatening complication from massive release of thyroid hormones, typically occurring within 1–2 days post-thyroidectomy in inadequately prepared hyperthyroid patients.

Incidence:

Occurs in 0.4–1.6% of patients

Mortality remains high if not promptly managed

Pathophysiology:

Sudden surge of T3/T4 into the bloodstream

Leads to adrenergic hyperactivity, cardiovascular collapse, multisystem failure

Adrenal decompensation may also occur

Precipitating Factors:

Surgery (esp. in thyrotoxic state)

Trauma, infection, DKA

Radioiodine therapy

Clinical Picture:

CNS: Agitation, delirium, psychosis, seizures, coma

CVS: Tachycardia (up to 200 bpm), atrial fibrillation, hypotension, acute heart failure

Skin: Hot, flushed, sweaty

GI: Nausea, vomiting, diarrhea, jaundice

Hyperpyrexia: Temp > 40°C (104°F)

May progress to thyrotoxic coma

Diagnosis:

Clinical—no definitive lab test

Burch-Wartofsky score or Japanese Thyroid Association scale helps estimate probability

Treatment:

GOALS: Block hormone synthesis/release, control symptoms, support organs

A.Suppress Hormone Release:

Lugol’s iodine IV (1% in NaI) after antithyroid drugs

PTU or methimazole (e.g., mercazolil 10 mg q8h)

B.Block Peripheral Effects:

Propranolol IV or PO (cautious in heart failure)

Reserpine may be used for sympathetic overdrive

C.Steroids:

Hydrocortisone 100–600 mg/day IV → for adrenal support, ↓ T4 to T3 conversion

D.Supportive Therapy:

IV fluids, oxygen, cooling measures

Sedatives for agitation

Cardiovascular support (digoxin, vasopressors if needed)

Detoxification: glucose, electrolytes correction

Prevention:

Always prepare hyperthyroid patients pre-op until euthyroid using:

o Antithyroid drugs (ATDs)

o Iodine preparations

o Beta blockers

oSteroids

Delay surgery until clinically and biochemically euthyroid

BLEEDING (Post-Thyroidectomy Hemorrhage) Incidence:

Occurs in 3–4%

One of the most feared early post-op complications

Intraoperative Bleeding:

Due to:

oSlippage of ligature or clip

oInjury to superior/inferior thyroid arteries, thyroid veins

Management:

oDo not clamp blindly

oFirst apply pressure, then clear field, identify source, ligate securely

Postoperative Bleeding:

May be external or internal

Mediastinal hematoma is dangerous — can cause:

oVagal stimulation → bradycardia

o Airway compression → stridor, suffocation

o Reflex cardiac arrest

Clinical Signs:

Neck swelling, pressure sensation

Dyspnea, tachycardia

Tracheal deviation, stridor

Hypotension, pallor Management:

Emergency bedside wound opening if airway is compromised

Immediate return to OR for hemostasis

Ensure drain placement in high-risk cases

RECURRENT LARYNGEAL NERVE (RLN) INJURY

Incidence:

Most common nerve injury in thyroid surgery

Occurs in 0.1–12.1%

Unilateral → hoarseness

Bilateral → airway obstruction, stridor → emergency tracheostomy

Mechanism:

Nerve is vulnerable during ligation of inferior thyroid artery

Can be:

o Transected

o Stretched

o Thermally injured

o Entrapped in scar tissue or ligature

Clinical Features:

Unilateral injury:

o Hoarse voice

o Weak cough

o Aspiration

Bilateral injury:

o Aphonia

o Stridor, respiratory distress

o Need urgent airway management

Diagnosis:

Indirect laryngoscopy (preand post-op mandatory in high-risk patients)

Flexible nasopharyngolaryngoscopy

Treatment:

Most resolve spontaneously within 1–2 months

Medications: Proserin, B vitamins

Voice therapy, vocal cord exercises

Persistent bilateral palsy → cord medialization surgery, tracheostomy

Prevention:

Visual identification of RLN during surgery is gold standard

Avoid blind clamping or ligation

9.Postoperative hypothyroidism, postoperative hypoparathyroidism.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Complication

Onset

Symptoms

 

Labs

 

Treatment

Prevention

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Days–

 

Tetany,

 

 

↓Ca² ,

 

 

 

IV Ca² ,

 

 

Preserve

 

weeks

 

paresthesia,

 

 

 

 

 

 

 

Hypoparathyroidism

 

 

 

↑PO ³ ,

 

 

 

oral Ca² ,

 

 

parathyroids,

 

post-

 

“obstetrician’s

↓PTH

 

 

 

vitamin D

 

 

autotransplant

 

op

 

hand”

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Early

Fatigue,

 

 

 

 

 

 

 

Leave enough

 

 

 

 

 

 

 

 

 

 

 

 

Hypothyroidism

or

bradycardia,

 

 

↑TSH,

 

 

 

L-

viable thyroid,

 

 

 

 

 

 

 

 

 

 

 

 

 

edema,

 

 

↓T4

 

 

 

thyroxine

avoid overt

 

months

 

 

 

 

 

 

post-

constipation

 

 

 

 

 

 

 

resection

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

op

1. POSTOPERATIVE HYPOPARATHYROIDISM

Definition:

A complication due to accidental injury, devascularization, or removal of the parathyroid glands, resulting in hypocalcemia.

Incidence:

0.1–2%

Higher in total thyroidectomy, thyroid cancer surgeries, or central neck dissection

Pathophysiology:

Parathyroids are small, delicate, and easily damaged or excised.

Their removal or ischemia disrupts PTH secretion, leading to: o ↓ PTH → ↓ serum calcium

o ↑ phosphate

o Possible vitamin D metabolism disruption

Clinical Presentation:

Latent (Subclinical) Tetany:

Positive Chvostek’s sign: facial twitching when tapping zygoma

Positive Trousseau’s sign: carpopedal spasm when inflating BP cuff on arm

Overt Tetany:

Paresthesias (fingers, toes, around mouth)

Cold extremities

Carpal spasms (“Obstetrician’s hand”)

Pedal spasms (“Horse’s foot”)

Muscle cramps, laryngospasm, seizures

Prolonged QT on ECG → risk of arrhythmias

Diagnosis:

Serum calcium

Serum phosphate

↓ or inappropriately normal PTH

Vitamin D level may be low, especially in winter

Treatment:

Conservative (Mainstay):

IV calcium chloride (10%) for acute tetany

Oral calcium supplements: calcium gluconate 6–10 g/day

Vitamin D (cholecalciferol or calcitriol):

o100,000–300,000 IU/day initially (adjust based on labs)

Magnesium: correct if low

Surgical/Experimental (Rare):

Calcium depot formation in severe cases

Parathyroid transplantation:

oHomotransplantation or autotransplantation into the sternocleidomastoid or forearm

Prevention:

Meticulous surgical technique to preserve parathyroids

Autotransplant parathyroid tissue if glands are removed or devascularized

Intraoperative PTH monitoring (if available)