новая папка / 450-550 operativ

Fig. 15-29: Hamburger – Brennan – Mahorner self retaining retractor with side arm to retract strap muscles.

Fig. 15-30: Retraction of the elevated aps in thyroidectomy using silk sutures.

ligated close to the gland to avoid injuring the nerve. Individual ligation of arteryand vein alsoprevents rare problem ofAV stula. Artery should have 2 or 3 zero vicryl ligatures proximally. Often clips/ligaseal device are used to the vessel.Slipping of the ligature postoperatively can cause life threatening haemorrhage or compressing haematoma. Often by many, superior pedicleis ligated enmass.Prior to thisKocher’s grooved director when available is passed underneath so that deeper tissues are safeguarded while cutting the pedicle. It is advisable to identify the external laryngeal nerve with careful dissection to safeguard it to prevent developing altered pitch of voice (timber of voice).

Inferior pole of the thyroid is exposed and inferior thyroid veins are ligated adjacent to gland. Often thyroid ima venous plexus may be present in front of the trachea in midline which should be ligated properly (Fig. 15-34).

Bothbluntand sharp dissectionusingpeanut, ne scissor, mosquito forceps with gentle traction over the gland medially will expose the recurrent laryngeal nerve and parathyroid glands. Recurrent laryngeal nerve passes behind the inferior thyroid artery in tracheooesophageal groove. But one should be aware of di erent variations which can cause nerve injury. Inferior thyroid artery arises from thyrocervical trunk of subclavian artery, running upwards, downwards and then medially under the carotid artery to reach the gland in front of the recurrent laryngeal nerve. To control any bleeders in this region bipolar cautery should be used (never unipolar). Branches of inferior thyroid artery while entering the gland should be ligated using 3 zero vicryl or silk. Ligating inferior thyroid artery or its branches close to gland avoids injury to the artery of parathyroid from inferior thyroid artery (capsular dissection or orange peel dissection). Olden day’s classical method of ligating the inferior thyroid artery away from the gland just after crossing behind the carotid artery (ligation in continuity using absorbable suture – catgut) is not commonly practiced now (Fig. 15-35).

Fig. 15-34: Ligation of superior thyroid artery is done close to the gland individually after identifying the external laryngeal nerve.

Fig.15-35C

Figs 15-35A to C: Location of parathyroids and their variations should be remembered. Parathyroids should be retained during thyroidectomy. It is also important to retain their blood supply also.

Fig. 15-36: Recurrent laryngeal nerve should be identi ed in all thyroidectomies.

Proper haemostasis is done using bipolar cautery. Pedicles are inspected again for their security (Fig. 15-39).

Closure

Sandbag is removed. Again haemostasis is con rmed. Often stretched neck prevents bleeding from small veins but once sandbag is removed they may bleed which should be controlled. Traditionally suction

Fig. 15-37: Partial or subtotal thyroidectomy is done by applying series of haemostats on the thyroid capsule to facilitate the removal of the gland in front. Retained gland is under run using vicryl sutures.

Fig. 15-38: Isthmus at its junction to retaining lobe of the thyroid gland is transected between clamps and retaining cut part of the thyroid tissue is under run using vicryl.

drain is placed which is brought out through a separate stab incision or one of the ends of the main wound. Drain should pass under the strap muscles to reach the thyroid fossa. If proper haemostasis is done draincan be avoided. Controversy still surrounds the use of drains after thyroid surgery. Strap muscles are approximated using interrupted 3 zero vicryl sutures. Platysma is sutured using 3 zero vicryl interrupted sutures. Subcuticular absorbable 3 zero monocryl suture is used for skin. Dressing with pressure using dynaplast is the usual practice. But a dressing that covers the wound may mask haematoma formation, delaying its recognition. Placing soft light dressing or without any dressing may be ideal even though it is not practiced by most surgeons

(Fig. 15-40).

The prevention of postoperative bleeding depends on good intraoperative hemostasis. Hemostasis in thyroid surgery is achieved by means of clamp and tie, surgical clips, diathermy - unipolar initially

Fig. 15-41: Bipolar cautery is used in deeper dissection. Monopolar cautery is used only during raising aps and incising the deep fascia in midline. Often argon laser coagulation may be used on the surface.

Fig. 15-42: Thin linear scar usually forms after thyroidectomy which is cosmetically acceptable.

Lateral Approach Thyroidectomy

Lateral approach is used in large thyroid enlargement/recurrent thyroid disease/often thyroid carcinoma instead of classical neck approach. After lengthy skin incision, plane is created between anterior border of sternomastoid muscle and lateral to strap muscles to proceed with surgery. Often sternocleidomastoid muscle may need to be removed.

Removal of Retrosternal Goitre

Usually there will be enlarged neck thyroid of similar pathology. As retrosternal thyroid receives its blood supply from neck it is usually delivered to thyroid incision of neck with blunt dissection and removed. Occasionally in large/vascular/adherent retrosternal goitre a median sternotomy may be added to remove it.

Postoperative Care

Patient is kept in postoperative room with head end tilted 30° upwards. Once patient is fully awake with normal breathing (in 4-6 hours), patient is shifted to ward. Patient should be observed for bleeding, formation of haematoma, stridor, drop in O2 saturation, tachycardia or tachypnoea. Tetany may be observed in 3-4 days. Hungry bone syndrome can cause severe hypocalcaemia in immediate postoperative period. Drain is removed in 24–48 hours depending on the quantity of collection in drain.

Remember in thyroidectomy

•Middle thyroid veinis present only in 30% of cases.

•Bipolar cautery or harmonic scalpel (harmonic wave)are better to controlbleeding and to prevent injury to RLN

•RLNshould be identified in both sides. Variations shouldbe remembered.

•Parathyroids should be retained and also their blood supply.

•Parathyroid autotransplantation may be needed if their blood supply is compromised.

•Rapidinflux of serum calcium into bones in immediate postoperative period may cause severe hypocalcaemia – hungry bone syndrome which is initially corrected by IV calcium gluconate – 10ml of 10%. It is more commonly observed in patients with beta blockers. Itis due to sudden dropin PTH level after surgery.

•Tension haematoma under strap muscles is very dangerous and should be relieved by removing sutures fromthe skin and strap muscles. It canbe life saving with immediate intervention otherwise it can be life threatening.

•Permanent hypoparathyroidism is rare (0.5-1%) even though temporary hypoparathyroidism and hypocalcaemia is common (25%) which is corrected well with calcium for certain period of 3-6 months.

•External laryngeal nerve injury is more commonthanRLN injury. There is loss of tension of vocal cords causing reduced power and range in voice (pitch).

•Thyroid insufficiency develops in 25-45% cases. It is confirmed by doing serum T3, T4 and TSH after 2, 3 and 6 months.

ward by the monitoring nurse or intensivist. Early identi cation of the problem with immediate bedside removal of skin and deeper sutures prevents further compression of the trachea relieving the respiratory obstruction. US of neck may be useful but unnecessary time should not be wasted just to do sonology. It is essentially life saving procedure which is often failed to undertake causing mortality. Later patient is shifted to operation theatre and wound is inspected under anaesthesia; bleeding vessel is caught and securely ligated. Often transfusion of blood is also required.

Respiratory Obstruction

It may be due to haematoma or due to laryngeal oedema or due to tracheomalacia or due to bilateral recurrent laryngeal nerve palsy. Evacuation of clot, emergency tracheostomy is required. Fiberoptic laryngoscopy is useful to assess the vocal cord palsy.

Recurrent Laryngeal Nerve Palsy

It can be transient or permanent. During extubation anaesthetist should be asked to visualise the movements of vocal cord to con rm that there is no recurrent laryngeal nerve injury. It should be documented both by anaesthetist and surgeon in the case sheet. Distressing change in voice should be assessed and treated by steroid (in case of neuropraxia), speech therapy and counseling. In malignant condition it is better to inform the patient about voice change as there would be possible need for transecting the nerve to clear the disease. However in benign diseases, nerve should be retained with all care. If nerve injury is identi ed on table during the procedure it should be repaired using microscope with 9 zero polypropylene sutures. Incidence of transient RLN palsy is 3%. It usually recovers in 3 weeks to 3 months. Permanent palsy is rare but do can occur. RLN palsy can be – unilateral; bilateral; unilateral combined RLN and external laryngeal nerve palsy; bilateral combined RLN and external laryngeal nerve palsy (Fig. 15-43).

Unilateral RLN palsy causes median or paramedian vocal cord position. Here all intrinsic muscles of larynx except cricothyroid on one side are paralysed. Cricothyroid, which is the only retained muscle is a weak adductor of the vocal cord causing median or paramedian

COMPLICATIONS OF THYROIDECTOMY

Complications can be intraoperative or immediate/in early postoperative period or late postoperative.

Haemorrhage (1%)

It may be due to slipping of ligatures either of superior thyroid artery or other pedicles or of small veins. It is often precipitated by vigorous coughing or retching in postoperative period. It causes tachycardia, hypotension, and breathlessness, tracheal compression due to progressive tension haematoma formation in thyroid fossa under sutured strap muscles causing severe respiratory obstruction, cyanosis, hypoxia, respiratory failure and cardiac arrest. Tension haematoma is a condition which is often missed in postoperative

Fig. 15-43: Recurrent laryngeal nerve should be identi ed in all thyroidectomies and safeguarded.

position of vocal cords (Wagner–Grossman hypothesis). Abductor bres (nerve supply of posterior cricoarytenoid) of the RLN which are phylogenetically newer are more susceptible and paralysed than adductors (Semon’s law). It causes change in voice (hoarseness) which gradually gets corrected by compensatory action of opposite vocal cord. Speech therapy will bene t for these patients. Short course of steroid in immediate postoperative period is used. 33% of unilateral RLN palsy patients are asymptomatic. Aspiration and airway obstruc-

tion will never occur (Fig. 15-44).

Unilateral combined RLN and superior laryngeal nerve palsy - All muscles of larynx on one side is paralysed. Vocal cord will be in cadaveric position, 3.5 mm from the midline. It leads into hoarseness of voice, ine ective glottis causing aspiration, ine ective cough and respiratory congestion. Treatment is speech therapy, Te on injection to paralysed vocal cord, placement of muscle/cartilage implant to paralysed cord, arthrodesis of cricoarytenoid joint.

Bilateral RLN palsy – Both side intrinsic muscles of larynx are paralysed except cricothyroids. Unopposed actions of both cricothyroids cause vocal cord in median/paramedian position. Condition causes voice change, severe dyspnoea, airway block and respiratory arrest. Treatment: Emergency tracheostomy; lateralisation of cord by arytenoidectomy; vocal cord lateralisation, cordectomy by open or laser method; sternohyoid implantation; thyroplasty.

Bilateral combined RLN and superior laryngeal nerve palsy – Here there will be total paralysis of the intrinsic muscles of larynx and total laryngeal anaesthesia, causing aphonia (no voice), severe glottis incompetence causing aspiration, absence of cough, retention of lung secretions leading into severe distress. It is treated by emergency tracheostomy, xing epiglottis to arytenoids, vocal cord plication and often by total laryngectomy.

Assessing the vocal cord palsy – It is done by indirect laryngoscopy, direct fibreoptic endoscopy, laryngeal electromyography (EMG). EMG may be useful to distinguish vocal fold paralysis from injury to the cricoarytenoid joint secondary to intubation. EMG may help in assessing the prognosis of the patient with RLN injury.

ick connective tissue called the Berry ligament attaches the thyroid to the trachea at the level of the second or third tracheal ring. is is the most common site of injury to the RLN. e nerve may run deep to the ligament, pass through it, or even penetrate the gland a short distance at this level. Retraction of the thyroid lobe may result in traction injury and make the nerve susceptible to transection. e path of the nerve

Fig. 15-44: Different vocal cord positions and also RLN palsy.

must be clearly identi ed. An endotracheal-tube electrode and an RLN-postcricoid-laryngeal surface electrode may be used in di cult thyroid surgeries to have continuous electrophysiologic monitoring to reveal the location of RLN. Proper identi cation of the RLN minimises the risk of injury. During thyroidectomy, when the nerve is identi ed and dissected, the reported RLN injury rate is 0-2.1%; if surgery is repeated (re-thyroidectomy) it is 2-12%; if the nerve is not identi ed it is 4-6.6%. Intraoperative haemostasis and a thorough understanding of the anatomy are essential for identifying and preserving the nerve.

For unilateral vocal cord paralysis corrective procedures are not done until at least 6 months after thyroidectomy because a reversible injury improves by that time. If the nerve was de nitely transected during surgery, treatment for the paralysed fold may be performed sooner than this.

Medialisation of the vocal cords is the most commonly performed. Medialization of the impaired vocal fold improves contact with the contralateral mobile fold. It is done by injection laryngoplasty or laryngeal framework surgery. Type I thyroplasty is probably the most common procedure. A window in the thyroid cartilage is created at the level of the true vocal fold. An implant is then placed to push the vocal fold medially. Medialization with an injection of absorbable gelatin sponge may be performed before 6 months. But gelatin sponge gets absorbed after sometime and is a temporary treatment.An implant made of silicone or polytetra uoroethylene is permanent. e implant may be removed if nerve function recovers later.

Reinnervation procedures are done for permanently injured RLN. ese procedures maintain/restore tone of the intrinsic laryngeal muscles. When the true vocal fold atrophies after denervation, it loses contactwiththe contralateralfoldandthevoiceweakens.Bypreventing atrophy, re-innervation procedures help to improvethe patient’s voice. Primary neurorrhaphy is done immediately to repair the transected

RLN.

In bilateral vocal-cord paralysis, initial treatment involves obtaining an adequate airway by emergency tracheotomy. Often rst endotracheal intubation is done; neck is explored to ensure that there are no reversible causes of nerve injury; if RLNs show good preservation, a trial of extubation may be performed after several days. Intravenous steroids are used. If nerve function has not recovered after a second trial of extubation, tracheotomy is certainly needed.

In bilateral vocal cord paralysis in order to improve airway patency, cordotomy and arytenoidectomy are the common procedures done. ese procedures enlarge the airway and allow de-cannulation of a tracheostomy. However, the patient must be counseled that his or her

voice will likely worsen after surgery.

Hypoparathyroidism—Types

Types

e parathyroid glands produce parathyroid hormone (PTH), which is involved in the regulation of serum calcium. PTH increases serum calcium levels by causing bone resorption, increasing renal absorption of calcium, and stimulating the synthesis of the biologicallyactive form of vitamin D (1, 25-dihydroxy vitamin D). 1, 25-dihydroxy vitamin D increases serum calcium levels by increasing the intestinal absorption of calcium. PTH also increases renal excretion of phosphorous. Low PTH levels result in high serum phosphorous levels.

Inadequate production of PTH leads to hypocalcaemia. Hypoparathyroidism, and the resulting hypocalcaemia, may be permanent or transient. e rate of permanent hypoparathyroidism is 0.4-13%. Causes are - direct trauma to the parathyroid glands, devascularisationof theglands, or removal of theglandsduringsurgery.

The rate of temporary hypocalcemia is reportedly 2-50%. The cause of transient hypocalcaemia after surgery is due to temporary hypoparathyroidism caused by reversibleischaemia to theparathyroid glands, hypothermia to the glands, or release of endothelin-1. Endothelin-1 is an acute-phase reactant which suppresses PTH production. Other hypothesis is - calcitonin release and hungrybone syndrome. Calcitonin is produced by the thyroid C cells which inhibits bone breakdown while stimulating renal excretion of calcium (opposite of PTH).

Risk factors for hypocalcaemia after thyroidectomy include Graves disease, malignancy, type of procedure performed (total thyroidectomy, thyroidectomy with neck dissection, repeat thyroidectomy, subtotal thyroidectomy, near-total thyroidectomy).

Initially asymptomatic for 4-5 days, later develop circumoral paresthesia/numbness, change in mental status, tetany, carpopedal spasm,Chvostek’s sign (tapping the region of the facial nerve in the preauricular area results in facial contractions), Trousseau’s sign (carpal spasm that is elicited by in ating blood pressure cu on the upper arm), laryngospasm (stridor), seizures, prolongation of QT on ECG, and cardiac arrest.

An effective method of evaluation of parathyroid function is to assess ionised calcium (or total calcium and albumin) levels in the perioperative period. A normal postoperative PTH level can accurately predict normocalcaemia after thyroid surgery. Immediate postoperative PTH level if <1.5 pmol/l and morning serum calcium <2.0 mmol/l, then patient is at risk of hypocalcaemia. Other causes like renal failure, hypomagnesaemia, medications should also be considered. Serum phosphorous levels are elevated in patients with hypoparathyroidism secondary to decreased renal excretion; this di erence may help in distinguishing low PTH levels due to other etiologies of hypocalcaemia. PTH levels may be checked repeatedly till 6 months during the follow up period. Identifying the glands on table and maintaining their blood supply is essential and also crucial to prevent hypoparathyroidism. 77% of superior parathyroid glands were at the cricothyroid junction and intimately associated with the RLN; 22% were on the posterior surface of the upper lobe of the thyroid; 1% was behind the junction of the hypopharynx and upper oesophagus.

Location of the inferior parathyroid glands was variable. 42% were on the anterior or lateral surfaces of the lower lobe of the thyroid, hidden byvessels or creases inthe thyroid;39% were located within the superior tongue of the thymus. 15% were extra-thyroidal and lateral to the lower lobe; 2% were in the mediastinal thymus; another 2% were in other ectopic positions, such as in the carotid sheath.

e inferior parathyroid glands and the thymus both develop from the third branchial pouch, causing close association of these structures. e inferior parathyroid glands receive their blood supply

is needed during discharge for 6 months. Postoperatively they need calcitriol (gradually increased to 16 mg in 1 month, then gradually