thyroidectomy morbidities
TRANSCRIPT
THYROIDECTOMY MORBIDITIES:Preventions & Interventions
ORLINO C. BISQUERA, JR., MD, FPCSDivision of Surgical Oncology, Head & Neck, Breast, Soft
Tissue and Esophago-Gastric SurgeryDepartment of Surgery, UP-PGH
Objectives• Discuss the different thyroidectomy morbidities
with its related anatomy, mechanism of injury,prevention & intervention.– Wound complications
• Hemorrhage• Hematoma• Seroma• Infection
– Nerve injury• Superior layryngeal nerve• Recurrent Laryngeal nerve
– Metabolic Complication• Hypocalcemia
– Other neck injuries• Tracheal injury• Esophageal injury
Wound Complications: Hemorrhage
• Uncommon• Life-threatening - < 1%• Factors for blood loss
– Venous hypertension– Diffuse goiter with increased vascularity– Substernal or intrathoracic goiter– Aberrant blood supply– Anatomical non-familiarity / poor
surgical technique
Hemorrhage: Possible Sources• Anterior jugular
veins• Thyroid vessels
– Superior & Inferior– Middle thyroid– Lobar vessels
• Aberrant bloodsupply
• Absent inferior thyroidartery: 2% - 5%
• Blood supply frombranches of the leftsubclavian artery
Hemorrhage: Potential problems
1. Obscuresidentification ofRLN and
Parathyroidglands
2. Hypotension /Death
High risk for hemorrhage
• Ectopic Goiters– Substernal goiter: More common
– Cervical goiter with enlargement towardsmediastinum
– Blood supply from inferior thyroid artery
– Mediastinal goiter: rare– Intra-thoracic blood supply
Problems:• Control of the inferior thyroid or intra-thoracic
blood supply• Venous hypertension from superior vena cava
compression
Intraoperative Hemorrhage:Prevention
1.Careful attention to surgical technique2.Anticipate potential high risk group
Substernal/Mediastinal goiters Careful planning in surgical approach
Cervical incision alone: Majority With sternotomy: 2% - 6% Extensive Mediastinal extension Mediastinal goiter
Excessive bleeding over avoidance of sternotomy
Hemorrhage: Intervention
Patient’s statusIdentified
source
Stable vital signs Unstable vital signsHypotension
Bleeding vesselIdentified
Excessivebleeding
precludesIdentifying source ofbleeding
*Ligate / repairbleedingvessel
Identify sourceof bleeding
Adequate exposureProximal / distal control
*Ligate / repairbleedingvessel *Resuscitation Effective gauze pack
Resuscitaion
Wound Complication: Hematoma• Incidence: 0% -3%• Factors: Inadequate hemostasis Increased venous pressure - coughing / straining on extubation Bleeding points:
– Temporarily coagulated small vessels– Residual thyroid gland (subtotal / Ligament of berry)– Major arteries and Veins
Hematoma: Manifestations• Majority: within 4 hours
post-op– Neck pain– Swelling with or without
echymosis– Continuous soaking of
dressing– Respiratory distress - “Bull
neck hematoma”• Laryngeal edema from venous
compression• Tracheal compression
– Hypotension
Hematoma: Prevention• Careful attention to
hemostasis before closure– Secured suture knots– Judicious electrocautery use
• Valsalva maneuver• Cough reflex- airway
suctioning– Increase venous pressure– Fills collapsed veins
• Drains / Bulky dressings– Not prevent hematoma– Delay recognition
Hematoma: InterventionKey: Early intervention
1. No airway compromise OR exploration & evacuation
Patient not left alone until hematoma is evacuated
2. Airway compromise (Bull neck) A. Initial bedside intervention
– Release skin,subcutaneous & strapmuscle closure
– Endotracheal intubation B. Operating room exploration &
evacuation
Wound Complication: Seroma
• Incidence: 0% -6%• Cause: Large dead space -Graves disease -Substernal goiter -MCAGPrevention: Placement of drainIntervention: Percutaneous aspiration
Wound Complication: Infection
• Incidence: <2%• Clean operation
– Drain / antibiotic: No effect on infection– Cause: Break in sterile technique Staph aureus
• Intervention– Appropriate antibiotics– Adequate drainage
Morbidity: Nerve injuries
1. SuperiorLaryngealnerve
2. RecurrentLaryngealnerve
Nerve Injury: Superior Laryngeal Nerve
Incidence: 0% - 20%Risk: Proximity to
superior thyroidvessels
Related anatomy:Vagus nerve - SLN Branches: Internal
branch External branch
Not visualized: 25%
Superior laryngeal nerve: anatomy
Internal branch: pierces thethyrohyoid membrane
Sensory innervation-laryngeal mucousmembrane
External Branch: closeassociation with superiorthyroid artery lateral toinferior pharyngealconstrictor
Diverge from the arteryat the upper border of thethyroid lobe to innervatethe cricothyroid muscle
Superior laryngeal nerve injury:manifestation
• Paralysis of cricothyroidmuscle– Lengthen and tenses the
vocal cords• Subtle voice changes• No airway compromise• No hoarseness but
restricted vocal range– Inability for high pitch
• Easy vocal fatiguability– Vocal cord tension
depends only frominternal laryngealmusculature
• Tolerated by mostpatients
• Career-threatening
CRICOTHYROID MUSCLEIntrinsic laryngeal muscleOrigin: side of cricoid cartilageInsertion: Thyroid cartilage lamina & inferior cornuAction: Vocal cord tension
Superior laryngeal nerve injury: Prevention
• Ligate superiorthyroid vesselclose to thethyroid lobe– Individual branch
ligation– Dissection from
medial to lateraldirection whilethe superior poleis retractedinferiorly
Superior laryngeal nerve injury:Intervention
• Delicate terminal fibersof external laryngealnerve– Cannot be repaired
• Speech therapy– Value is limited but may
help in laryngealcompensation
Recurrent laryngeal nerve injury
• Incidence:– Unilateral nerve injury
• Permanent: 1% - 1.5%• Temporary: 2.5% - 5%
– Bilateral nerve injury• Rare
• High Risk: Advanced disease
Recurrent laryngeal nerve:Anatomy
Origin: Vagus NerveRight: recurs behind the subclavian arteryLeft: recurs behind the aortic archNerve courses upward via the tracheoesophageal grooveEnters the larynx at the cricothyroid joint areaFunction: Innervation of internal laryngeal musculature
Non-recurrent: 1%
Recurrent laryngeal nerve:Landmarks for identification
Relationship to inferior thyroid artery Posterior: 50% Between branches: 25% Anterior: 25%
Relationship with inferiorthyroid cornu RLN laryngeal entry: 1 cm below the inferior thyroid cornu (palpable) : constant landmark for RLN identification
Recurrent laryngeal nerve:Mechanisms of injury
• Stretch• Swelling• Transection• Ligation
Recurrent laryngeal nerve injury:Manifestations
• Unilateral injury– Voice limitation and hoarseness– Usually with no airway compromise– Pre-op laryngeal evaluation to determine relationship with thyroidectomy– Rarely with aspiration
• Bilateral injury– Spastic phase
• Adduction of the vocal cords• Airway obstruction after extubation (stridor)
– Relaxation phase• Abducted bilateral vocal cords
– high risk for aspiration– Weak voice
• Slowly the vocal cords assumes paramedian position– Improvement of voice but with more airway compromise
Recurrent laryngeal nerve injury:Preventions
• Good surgical technique• Visualization of its entire course
– Anatomical familiarity• Susceptible areas for injury
1. Ligament of berry– Attaches part of thyroid tissue to the trachea– Closest contact between the nerve & thyroid tissue– Usually RLN courses posterior to it
– 25% courses through it2. Inferior thyroid artery
Posterior: 50% Between branches: 25% Anterior: 25%
ANTERO-MEDIAL RETRACTION OF THYROID
Recurrent laryngeal nerve injury:Intraoperative Intervention
• Nerve ligation• Release ligature
• Unilateral nerve transection• Immediate microsurgical repair
–Prevents vocal cord atrophy• Bilateral nerve transection
• Immediate microsurgical repair• Tracheostomy
Recurrent laryngeal nerve injury:Postoperative Intervention
• Unilateral vocal cord paralysis• Nerve visualized & preserved:
– Supportive– Anticipate return of function in 3 – 6
months• Nerve transected & not repaired
– Laryngoplasty or vocal cordinjection
» Stiffen and medialize the cord» Allow contralateral cord to
appose during speech
Recurrent laryngeal nerve injury:Postoperative Intervention
• Bilateral vocal cord paralysis– Provide more airway while maintaining voice– Options:
• Irreversible procedures– Arytenoidectomy– Transverse cordotomy
» Widens airway» No improvement in voice quality
• Timing: 1 year post-injury
Metabolic Complication:Hypocalcemia
• Temporary: 0.3% - 49% Symptomatic within 2 weeks Resolves within 6 months• Permanent: 0% - 13% Requires calcium / vitamin D to maintain normal calcium 1 year after thyroid surgery
Hypocalcemia after thyroidsurgery: Causes
• Devascularization: direct injury of blood supply or indirectly from hematoma
• Inadvertentremoval ofparathyroid gland
Parathyroid glands: Relatedanatomy
• Vascularsupply
• 90% inferiorthyroid artery
• 10% superiorthyroid artery
Parathyroid glands: Related anatomy
Embryology & LocationsSuperior 4th Branchial pouch Descends with the thyroid Posteromedial surface of the thyroid between upper & middle 3rdInferior 3rd Branchial pouch Descends with the thymus Within a circle ( 3 cm diameter) center is where RLN intersect the inferior thyroid artery
Postoperative Hypocalcemia:Manifestations
• Normal serum calcium: 8.5 -10.5 mg/dl• Symptomatic hypocalcemia: <8 mg/dl• Mild symptoms
– Numbness/ tingling: lips, hands & feet• Chvosteks’s sign – involuntary contraction of
facial musculature upon tapping of cheek overfacial nerve
• Trousseau’s sign- carpal spasm uponocclusion of arm blood supply to systolicpressure for 2 minutes
– Painful procedure, usually not done
Symptomatic Hypocalcemia:Late symptoms
• Untreated initial symptoms• Severe symptoms
– Mental status changes-irritability,disorientation
– Muscle cramps & spasm– Hypotention– ECG-prolongation of Q-T interval– Laryngospasm– Seizure
• Medical emergency
Hypocalcemia: Prevention– Routine identification
of parathyroid glands– Preservation of
parathyroid bloodsupply
• Ligate branches ofinferior thyroid arteryclose to the thyroidgland (tertiary branches)
• Preserve if there isblood supply fromposterior branches ofthe superior thyroidartery
– Careful dissection ofparathyroid gland offthe thyroid capsule
Parathyroid injury: IntraoperativeIntervention
• Questionable viability: duskyparathyroid gland– SCM autotransplantation
• More predictable function than non-viable gland left in situ
• Lowers incidence of permanenthypoparathyroidism
Parathyroid autotransplantation:The technique
• Fragment of non-viabletissue is sent for frozensection confirmation– Mince the other fragments
to 1 mm pieces and place inSCM pocket. Close theoverlying SCM fascia withsuture
• Graft success rate: 50% -100%
• Autotransplanted glandrevascularization: 3 – 6weeks
Postoperative Hypocalcemia:Intervention
• Mild symptoms: requires prompt calciumreplacement– Prevents progression to severe tetany– 15 mg elemental calcium/ kg/dayOral calcium supplementation 2 – 10 gms / day in divided dose (b.i.d – q.i.d )
• Calcium carbonate 650 mg tab = 250 mg elemental calcium• 70kg X 15 =1050 mg elemental calcium/ day = 4 tablets• 2 tabs b.i.d
Oral Calcium Supplement: Needfor Vitamin D
• Inability to maintain Serum calciumabove 8 mg/dl with oral calcium alone
• Oral calcium supplement is requiredbeyond 4th post-op day– Oral calcium dose > 3gms / day– Calcitriol (1,25 dihydroxy vitamin D) p.o.
• BID with 0.5 – 1.0 ug total daily dose– Increase GIT Ca absorption
• Severe symptoms• 10%Calcium gluconate 10 – 30 ml slow IV over 10
minutes– Repeat dose if necessary to reverse symptoms (maintain serum
calcium above 8 mg /dl)– Effect diminishes after 2 hours
• 10% Ca gluconate drip (0.5 – 1.5 mg elementalcalcium/Kg/hr)
• 6 ampules = 6 gms calcium = 558 mg elemental Calcium in in 500 ml D5W• Infusion at 1 ml / Kg / hour over 8 -24 hours• Provides steady calcium supplement while oral calcium is being
absorbed• Monitor calcium q 4 hours• Discontinue drip: Ionized calcium > 1.12 mmol/L
Start oral calcium at once
Postoperative Hypocalcemia:Intervention
Other neck injury: Trachea• Large invasive tumors• Careless dissection of thyroid
from trachea• High risk area: Ligament of berryPrevention: Anterior retraction of
thyroid lobe & isthmus whilepressing trachea downward
Avascular pretracheal planeIntervention:
1. Primary repair2. SCM patch = >1cm defect3. Resection & primary
anastomosis4. Tracheostomy through defect
SCMflap
Resection &anastomosis
Other neck injury: Pharynx /Esophagus
• Rare• Invasive carcinomaPrevention: Gentle dissection Correct dissection plane Anatomical anticipation NGT as esophageal guideIntervention:
Primary repairExtensive esophageal loss
Flap: SCM / pect major Jejunal interposition
SUMMARY• Thyroidectomy morbidities
– Wound complications• Hemorrhage• Hematoma• Seroma• Infection
– Nerve injury• Superior layryngeal nerve• Recurrent Laryngeal nerve
– Metabolic Complication• Hypocalcemia
– Other neck injuries• Tracheal injury• Esophageal injury
Anatomy,mechanism ofinjury,prevention& intervention
Morbidity in thyroidectomy
The best intervention is still PREVENTION!
Division of Surgical Oncology, Head & Neck, Breast,Soft Tissue and Esophago-Gastric Surgery
Department of Surgery, UP-PGH
Serum Calcium• Total serum calcium
– Dependent on serum protein for binding– Low protein Low total serum calcium
– Not reflective of active IONIZED calcium– Correction: Decrease of 1 gm/dl serum protein
• Ionized Calcium: Free– Hypocalcemia: severe - < 1.0 mmol / L mild – 1.0 - 1.12 mmol / L (4.0 mg / dl)
Corresponding Decrease of Total serum calcium of 0.8 mg/dl
IV Calcium administration
• 10% Calcium gluconate slow IV 5 minutes• 10% Ca gluconate drip
• 6 ampules = 6 gms calcium = 540meqs Calcium in in 500 ml D5W• Infusion at 1 ml / Kg / hour• Provides steady calcium supplement while oral
calcium is being absorbed
• Check Magnesium level– Hypo: Impairs PTH secretion Increases PTH resistance
Calcium carbonate tablet: MildHypocalcemia
• 650 mg tab = 250 mg elemental calcium• Treatment: 15 mg / kg / day
• 70kg X 15 =1050 mg / day = 4 tablets• 1 tab q.i.d
Calcium gluconate drip: SevereHypocalcemia
• 100mg / ml X 10 ml ampule = 1 gm Ca = 93 mg ofelemental calcium
• 93 X 6 ampules = 558 mg elemental calcium• Mix in 500 cc D5W = 1mg /ml
• 70 kg x 0.5 mg elemental calcium/kg/hr = 35mg• 35 ugtt /min = 35 cc / hr = 35 mg /hr
• Objective: 0.5 -1.5 mg elemental calcium /kg/hr infusion over 8 -24 hours : Discontinue infusion – Cai >1.12 mmol/L• Measure ionized calcium q 4 hours