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Acinic Cell Carcinoma (AcCC) of the Salivary Glands

• Acinic cell carcinomas (AcCC):

• Is the second most common malignant tumor:

• Involving the parotid gland

• They represent 15% of malignant parotid gland neoplasms

• AcCC accounts for approximately:

5% to 17% of all salivary gland tumors:

• 10% to 17% of all malignant salivary gland tumors

• The parotid gland is composed almost exclusively of serous type acini:

• And it is the most common site of AcCC:

• 80% to 90% of cases

• Other reported sites are:

• The palate (up to 15%)

• Submandibular gland (4%)

• Sublingual gland (1%)

• AcCC occurs most often in the fifth decade of life:

• Women are affected more often than in men (ratio 3:2)

• It is generally a low-grade carcinoma:

• With indolent behavior

• Recurrences are usually delayed:

• Sometimes after decades:

• In a series reported by Ellis et al:

• 12% of tumors recurred and 8% metastasized (bone, lung, and brain)

• The regional lymph nodes:

• Were the most common site of metastases:

• Spafford et al:

• Reported cervical lymphadenopathy to be present in 10% to 15% of cases of AcCC

• Spiro et al:

• In a series of 67 cases with AcCC treated before 1968, identified five cases (7.5%) with cervical metastases at the time of initial treatment

• It is interesting that this tumor is the most common bilateral malignant salivary gland neoplasm:

• Although its bilateral presentation is not nearly as common as the bilateral presentations of benign tumors:

• Warthin’s tumor and pleomorphic adenoma

• AcCC:

• Are typically encased in a fibrous capsule:

Grossly resembling round circumscribed nodules with a tan surface

• The cut surface is solid but may show cystic degeneration and hemorrhage

• Histologically, there are five cell types:

• Serous acinar cells:

• Explaining the predilection for the parotid gland

• Cells with clear cytoplasm

• Intercalated ductal cell

• Nonspecific glandular cell

• Vacuolated cell

• The microscopic recognition of AcCC also requires a strong appreciation for its varied growth patterns:

• There are four histologic growth patterns:

• Solid

• Microcystic

• Papillary

• Follicular

• Caution must be taken not to misread the:

• Solid pattern as normal parotid parenchyma

• The papillary-cystic pattern as cystic mucoepidermoid carcinoma

• The follicular pattern as metastatic thyroid carcinoma

• Serous acinar differentiation:

• Is developed most fully in the acinic cell:

• These cells have dark round nuclei and granular purplish cytoplasm

• The diagnosis of AcCC may be difficult to establish:

• Especially when some other cell type dominates the histopathology picture

• Some examples of this are the predominance of clear cells might cause confusion with:

• Mucoepidermoid carcinoma, clear cell adenocarcinoma, and metastatic renal cell carcinoma:

• In these circumstances, the diagnostic acinic cells can be identified using a periodic acid-Schiff (PAS) reagent:

• Their cytoplasmic secretory granules are PAS positive and diastase resistant

• Overall survival has been crudely estimated to be about 84%:

• Survival at 5 years has been reported between 76% to 90%, but fell to 56% at 20 years:

• Emphasizing the need for long- term follow-up

Toboggans Technique for Retrosternal Goiters a Valuable Technique to Protect RLN

  • Toboggans technique for retrosternal goitre a valuable technique to protect RLN:
    • The surgery of retrosternal goiter is at increased risk for iatrogenic recurrent laryngeal nerve lesion
  • Charles Proye:
    • Described a surgical technique to avoid this lesion
  • To have a better exposition, resection of the prethyroid muscles can be considered:
    • Particularly if it is a voluminous and / or recurrent goiter. 
  • The approach starts with:
    • The thyroid isthmus liberation that is dissected free from the anterior part of the trachea and transected
  • Then:
    • The middle thyroid vein is divided and the superior pole vessels are divided
  • The superior pole is then mobilized laterally:
    • And the recurrent laryngeal nerve is searched for at its entry point into the larynx
  • The nerve function can be verified by the neuromonitoring:
    • Which also helps to find it in this vessel-rich area
  • The dissection continues between the nerve and the posterior part of the thyroid:
    • Progressively from top to bottom:
      • Descending as on a toboggan
  • After the recurrent nerve dissection:
    • The goiter can usually be extracted without difficulty:
      • Dividing the last vessels holding the goiter inside

https://www.liebertpub.com/doi/full/10.1089/ve.2014.0009

Rodrigo Arrangoiz MS, MD, FACS thyroid and parathyroid surgeon at Mount Sinai Medical Center.

Surgical Training:

• General Surgery
• Michigan State University:
• 2005 to 2010image-48• Complex Surgical Oncology / Head and Neck Surgery / Endocrine Surgery:
• Fox Chase Cancer Center (Filadelfia):
• 2010 to 2012image-39• Masters in Science (Clinical research for health care professionals):
• Drexel University (Filadelfia):
• 2010 to 2012image-50• Head and Neck Surgery and Oncology
• IFHNOS / Memorial Sloan Kettering Cancer Center:
• 2014 to 2016

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Invasive Lobular Carcinoma of the Breast

Invasive Lobular Carcinoma of the Breast

  • Invasive lobular carcinoma:
    • Is the most common special histological subtype of invasive breast carcinoma
  • From an evolutionary point of view:
    • These tumors arise from a family of non-obligate precursor lesions called:
      • Atypical lobular hyperplasia (ALH) and lobular carcinoma in situ (LCIS):
        • Which may be collectively termed:
          • Lobular neoplasia (LN)
  • Even within this narrow spectrum of pre-invasive lesions and frank invasive carcinoma:
    • There is significant morphological and biological heterogeneity
  • The multistep model of breast cancer progression:
    • Contends that although lobular carcinomas:
      • Arise along the low-grade, ER-positive arm of the pathway (with low-grade, ER-positive ductal lesions):
        • De-differentiation to higher grade lesions: 
          • Can occur through acquisition of alterations in oncogenes such as:
            • ERBB2 and TP53:
              • Producing a spectrum of heterogenous proliferations
  • Lobular neoplasia (LN):
    • Are mostly an incidental finding:
      • Comprise neoplastic proliferation of characteristically discohesive cells:
        • Which fill and distend the terminal duct lobular units
    • LN encompasses both:
      • ALH and LCIS:
        • The boundary between the two is defined by:
          • An arbitrary cut-off using a quantitative measure:
            • Depending on the relative extent of involvement of the terminal duct lobular unit (TDLU):
              • If more than 50% of the TDLU is occupied:
                • The lesion is upgraded to LCIS
      • LN is considered to be a:
        • Non-obligate precursor of invasive cancer with:
          • ALH associated with a:
            • 4 to 5 times increased relative risk for subsequent cancer
        • LCIS associated with a:
          • 8 to 10 times increased relative risk for subsequent cancer:
            • The risk is bilateral:
              • But predominates for the ipsilateral breast
  • Classic invasive lobular carcinoma (ILC):
    • Typically demonstrates:
      • Single cell infiltration and a characteristic targetoid pattern of growth with minimal associated stromal response
    • This pattern of subtle invasion:
      • Is such that the size of the tumor often exceeds the imaging findings:
        • And obtaining clear surgical margins may be challenging
    • Although ILCs are generally palpable:
      • A high false-negative mammography rate is possible:
        • In 19% to 43%
    • In addition to the classic form of ILC:
      • Which is typically histological grade 2:
        • There are special morphological subtypes including:
          • Pleomorphic
          • Solid
          • Alveolar
          • Tubulo-lobular
      • These variants are rarely seen as pure form:
        • And are more likely to be present with the classical type
  • ILC and its subtypes are typified by:
    • A loss of cellular adhesion:
      • Frequently the result of biallelic inactivation (i.e. gene mutation combined with gene deletion) of the CDH1 gene:
        • Encoding E-cadherin:
          • Although other mechanisms of expression loss also feature
  • ILCs are normally estrogen (ER) and progesterone (PR) receptor positive:
    • And as such patients are indicated for hormone therapy
  • Whilst the biological characteristics of ILC afford patients a good prognosis in the short term:
    • It has become clear that the longer-term prognosis of ILC is frequently worse than for patients with the more commonly diagnosed invasive breast carcinoma of no special type (IBC-NST; invasive ductal carcinoma, IDC)
  • The metastatic presentation of ILC:
    • Has long been considered unique:
      • With a predilection for common sites (liver, lung, bone), but also gastrointestinal and gynecological sites of colonization:
        • Recent studies further support this:
          • Inoue et al. showed that lung metastases were less prevalent:
            • But peritoneal metastases are significantly higher in ILC (assumed predominantly classic ILC) compared to ER-positive IBC-NST
          • A recent study of metastatic spread to gynecological site:
            • Demonstrated an association with ILC and young age at diagnosis and confirmed earlier reports of the wide metastatic colonization of ILC
      • Immunophenotyping:
        • Showed a heterogeneous interplay between:
          • Hormone receptors and their co-factors during progression, including:
            • Frequent downregulation of PR expression and variable changes between AR, GATA3, and FOXA1 seen in different metastases within the same patient
  • Rarer presentations are increasingly being published in the literature:
    • Further highlighting the peculiar natural history of ILC:
      • For example, numerous case reports of ILC seeding as orbital metastases appear to suggest these are more likely to arise from an ILC than other types, and in a sole example of a mixed ductal-lobular carcinoma, only the lobular component was found in the orbital metastasis
  • The WHO Classificationrecognizes three variants of LCIS:
    • Classic (CLCIS)
    • Pleomorphic (PLCIS)
    • Florid (FLCIS) 
  • The defining features of both PLCIS and FLCIS have recently been clarified: 
    • PLCIS:
      • Is characterized by cells with enlarged nuclei (4× size of lymphocytes) or similar cytological features to those seen in high-grade ductal carcinoma in situ (DCIS)
  • FLCIS:
    • Is characterized by confluent expansive growth, and there must be marked distention of involved acini with little intervening stroma or an expanded acinus or duct approximately 40 to 50 cells in diameter
  • PLCIS is therefore characterized by its degree of cytological atypia:
    • Whereas FLCIS describes an architectural pattern (confluent, mass-like growth) with proliferation that is of classic type (CLCIS)
  • Unlike CLCIS, PLCIS and FLCIS are more likely to have:
    • Comedo-necrosis and calcifications and hence clinical and radiological presentations
  • CLCIS:
    • Is invariably ER and PR positive, and HER2 negative
  • FLCIS exhibits a similar phenotype:
    • Although may occasionally be HER2 positive
  • PLCIS exhibits a more varied phenotype:
    • With less frequent hormone receptor positivity, and an increased likelihood for HER2 overexpression:
      • Particularly in the apocrine-type of PLCIS as well as a higher proliferative index
  • The natural history of PLCIS and FLCIS:
    • Is as yet not well understood, and as such, relative risk of progression to frank invasive disease remains unclear, and we await long-term outcome data
  • An accumulating volume of work has investigated the molecular characteristics of CLCIS and these special subtypes:
    • The application of genomic technologies (copy number profiling, whole exome and targeted panel sequencing):
      • To a large set of LCIS confirmed that these lesions were frequently:
        • Clonally related to other more malignant lesions found to co-occur in the same specimen (i.e. DCIS and ILC):
          • And that intralesion molecular heterogeneity was also identified within LCIS:
            • Particularly among those lesions clonally related to DCIS and / or ILC
    • The data further supports the idea that:
      • LCIS shares molecular characteristics with its invasive counterpart:
        • Suggesting they do indeed have a common clonal origin:
          • And that LCIS is a non-obligate precursor of ILC
      • Considerable genomic diversity may arise in LCIS whilst the lesion is still confined within the ductal architecture:
        • Accounting for some of the morphological and biological variability observed on the progression to invasive cancer
        • Some of this intralesional LCIS heterogeneity:
          • Accounts for the occurrence of PLCIS and FLCIS
      • There is a striking similarity in the genomic profiles of CLCIS, PLCIS, and FLCIS (and invasive tumors):
        • With recurrent gains of 1q and losses on 16q and CDH1 mutations: 
          • Suggesting they arise from a common etiology
      • FLCIS and PLCIS with apocrine differentiation:
        • Are more genomically complex than CLCIS and non-apocrine PLCIS:
          • With an increase in the number of amplifications, genomic losses, and breakpoints
      • An increased frequency of ERBB2 / HER2 mutations or amplifications:
        • Has been reported in PLCIS compared to classic LCIS
Multistep model of the evolution of classic ILC and its morphological variants.
A lineage of ‘lobular’ disease evolves from a normal epithelial cell on a background of a loss of E-cadherin expression and function, and key early somatic alterations involving gain of chromosome 1q, loss of 16q, and mutations in PIK3CA, AKT1, or PTEN.
The morphological and molecular diversity of in situ and invasive lobular lesions is likely to be a result of the subsequently arising pattern of molecular alterations that drive progression.
Atypical lobular hyperplasia (ALH) is distinguishable from lobular carcinoma in situ (LCIS) based on the extent of proliferation within the lobule.
Pleomorphic LCIS (PLCIS) and florid LCIS (FLCIS) can emerge either from ALH (presumably) or from classic LCIS (CLCIS), with an increasing level of genomic
Histological examples of lobular variants.
a. CLCIS and CILC (as marked), × 40 magnification.
b. FLCIS shows the cytology of CLCIS with marked distention of lobular units to form a confluent mass-like lesion, × 40 magnification.
c. PLCIS with cytological atypia—nuclear pleomorphism with large vesicular nuclei and nucleoli—at least some × 4 the size of lymphocytes; × 600 magnification.
d. PILC, characteristic discohesion but with high-grade pleomorphic nuclei, with pink, foamy cytoplasm typical of an apocrine phenotype, × 400 magnification.
e. ILC with signet ring cell morphology, × 200 magnification.
f. Solid with sheets of classic type cells, × 200 magnification.
g. ILC showing mucinous / histiocytoid

#Arrangoiz #BreastSurgeon #CancerSurgeon #SurgicalOnologist #MSMC #MountSinaiMedicalCenter #BreastCancer #InvasiveLobularCarcinoma #ILC #LobularNeoplasia #Mexico #Miami

Thyroid Surgery Volumen and Outcomes

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  • Introduction: Although the association between annual surgeon total thyroidectomy volume and clinical outcomes is well established, published methods typically group surgeons into volume categories. The volume-outcomes association is likely continuous, but little is known about the point at which the annual surgeon procedure volumes begin to be associated with a decrease in complication rates.
  • Multiple studies have demonstrated the relationship between surgeon volume and improved patient outcomes.

  • This is no different for thyroid surgery; when procedures are performed by high-volume surgeons, patients have decreased rates of endocrine-specific complications (e.g., transient and permanent hypoparathyroidism and recurrent laryngeal-nerve injury), shorter hospital stays, and lower rates of readmission.

  • Previous studies have varied with respect to the definition of a high-volume surgeon, ranging from a threshold of 30 to 100 thyroidectomies per year:

    • One recent study demonstrated that the likelihood of experiencing a complication decreased with increased surgeon volume, up to 26 total thyroidectomies per year.

 

  • The intent of the current study was to examine the association between surgeon volume and patient outcomes for total thyroidectomy, with the hypothesis that the optimal threshold is continuous, with no defined cut point defining a high-volume surgeon.

Presentation1

2019 Jul 25. doi: 10.1001/jamaoto.2019.1752

 

¿Quién debe realizar cirugía de tiroides?

  • Generalmente debe ser cirujanos con sub-especialidades que tiene un volumen alto de casos por año:
    • No es ideal un cirujano general que realizar muy pocos casos al año
  • Estas sub-especialidades son:
    • Cirugia oncológica
    • Cirugia de cabeza y cuello
    • Cirugia endocrina
  • Les dejo la respuesta de Ashok R. Shaha, MD, FACS (profesor MSKCC / IFHNOS) en su presentación que dio en el Keynote Lectura del American Head and Neck Society:

prof_739_20190417135234

  • Rodrigo Arrangoiz MS, MD, FACS, FSSO miembro de Mount Sinai Medical Center cumple con los requisitos señalados por el Dr. Shaha:
    • El Dr. Arrangoiz tiene entrenamiento en: Cirugía de tumores de cabeza y cuello, cirugía endocrina, y cirugía oncológica.
  •  Su entrenamiento es el siguiente:

    • Tumores de Cabeza y Cuello / Cirugía Endocrina: Fox Chase Cancer Center

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  • Tumores de Cabeza y Cuello / Cirugía Endocrina:IFHNOS / Memorial Sloan Kettering Cancer Center

 

Cirugía Oncológica Compleja: Fox Chase Cancer Center

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  • Cirugia General y Gastrointestinal:
    • Michigan State University

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  • Maestría en Ciencias de Investigación:Drexel University

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  • El Dr. Arrangoiz esta certificado por:El Colegio Americano de Cirugía

Unknown

  • El Dr. Arrangoiz es: Fellow del Colegio Americano de Cirugía

 

El Dr. Arrangoiz es:

Fellow de la Sociedad de Cirugia Oncológica:

Unknown

  • Es miembro de la American Thyroid Association

Unknown

rodrigo.arrangoiz@gmail.com

#MountSinaiMedicalCenter

Secondary Hyperparathyroidism

  • Hyperparathyroidism is an inevitable feature of end-stage renal disease (ESRD):
    • It is a result of decreased renal tubular excretion of phosphate and defective 1-α hydroxylase enzyme:
      • Which cause impaired renal activation of 25-hydroxycholecalciferal to 1,25 dihydroxycholecalciferol
        • These causes hyperphosphatemia and hypovitaminosis D:
          • Which result in prolonged hypocalcemia:
            • That lead to hyperplasia of the chief cells of the parathyroid glands:
              • And eventually increased secretion of parathyroid hormone (PTH)
  • When the condition is chronic and prolonged:
    • The pathologic changes may become irreversible:
      • With skeletal resistance to PTH
      • Autonomous function of the hyperplastic glands:
        • Even with correction of the underlying cause and withdrawal of calcium and calcitriol therapy
  • Parathyroidectomy:
    • Is usually warranted in severe refractor renal hyperparathyroidism:
      • After failure of pharmacologic treatment with calcitriol, a vitamin D analog, or cinacalcet
    • The procedure is also considered when the medical therapy to reduce the level of intact PTH (iPTH):
      • Results in unacceptable elevation of the serum calcium and / or phosphorus:
        • With the potential for precipitation and increased cardiovascular mortality:
          • When the calcium-phosphate product exceeds 55 mg2/dl2) or when the adverse effects of the pharmacotherapy are not tolerated by the patient

#Arrangoiz #ParathyroidSurgeon #ParathyroidExpert #Hyperparathyroidism #Surgeon #HeadandNeckSurgeon #Teacher #MSMC #MountSinaiMedicalCenter #Miami #Mexico #EndocrineSurgery

Auto-Transplantation of a Parathyroid Gland

  • The auto-transplantation site is directed by the pathological condition directing bilateral neck exploration (BNE):
    • As a general rule of thumb:
      • If the devascularized gland is morphologically normal:
        • It is transplanted into the sternocleidomastoid muscle
      • If the devascularized gland is morphologically abnormal:
        • The gland is transplanted into a site remote from the operative field:
          • Such as the brachioradialis muscle
Procedure for auto-transplant into brachioradialis. These images demonstrate the steps taken to transplant an abnormal parathyroid gland into the right brachioradialis muscle of a patient with tertiary hyperparathyroidism. (a) A 2-cm incision is made over the brachioradialis muscle approximately 5 cm distal to the cubital crease. The dissection is continued down to the deep fascia, with care taken to identify and protect the posterior cutaneous nerve of the forearm (a). (b) The fascia is incised and a 1-cm pocket is created in the muscle. (c) The morcellated parathyroid tissue is placed into the pocket. (d) The fascia is closed, and the position of the auto-transplant is marked with a Hemoaclip at its proximal and distal extent, and a Prolene suture between these

#Arrangoiz #ParathyroidSurgeon #ParathyroidExpert #Parathyroidectomy #MSMC #MountSinaiMedicalCenter #HeadandNeckSurgeon #Surgeon #Teacher #EndocrineSurgery

Removal of Morphologically Abnormal Parathyroid Gland (s)

  • The gland is bluntly dissected from the surrounding tissue back toward its vascular pedicle, with particular care not to breach the capsule of the gland (Figure)
Exposure of the vascular pedicle. The gland has been dissected away from the surrounding tissue to expose its supplying vascular pedicle, which can then be ligated with a bipolar cautery or a small clip. The position of the recurrent laryngeal nerve, which can be seen in the bottom of the image, should be re-confirmed during this stage
  • The vascular pedicle is then ligated with bipolar cautery or a small clip:
    • After first re-confirming the position of RLN.
  • The excised gland(s) should then be sent to pathology
    • To confirm the weight and presence of parathyroid tissue, if available

#Arrangoiz #ParathyroidSurgeon #ParathyroidExpert #Parathyroidectomy #MSMC #MountSinaiMedicalCenter #HeadandNeckSurgeon #Surgeon #Teacher #EndocrineSurgery

Etiology of Goiters

• Etiology:

• Iodine deficiency:

• Is the most common cause of goiter worldwide

• In mildly and moderately iodine-deficient regions in Denmark:

• Goiter (as determined by ultrasonography) is present in 15% and 22.6% of the population, respectively

• In the United States, where significant iodine deficiency does not exist:

• Multinodular goiter, chronic autoimmune (Hashimoto’s) thyroiditis, and Graves’ disease are more common causes of goiter:

• In older adults, multinodular goiter is most common

• Other less common causes of goiter include:

• Tumors

• Thyroiditis

• Infiltrative diseases

• The risk of thyroid cancer within a multinodular goiter:

• Is approximately 3% to 5%:

Similar to the risk in a solitary thyroid nodule

• In a series of 718 patients operated on for goiter in Pakistan:

• 3% of patients were found to have a malignancy

• In a surgical series (with potential selection bias) of 3233 patients with multinodular goiter:

• In which all patients had preoperative ultrasounds and patients who had indeterminate, suspicious, or malignant (Bethesda 3 to 6) preoperative FNA were excluded:

• 31.7% had incidental thyroid cancers:

• Of which 56% were papillary microcarcinomas

• Pathophysiology:

• In patients with iodine deficiency or chronic autoimmune (Hashimoto’s) thyroiditis:

• An increase in thyroid-stimulating hormone (TSH) secretion:

• Is the predominant cause of goiter

• In contrast, most patients with sporadic nontoxic multinodular goiters:

• Have normal serum TSH concentrations:

• In these individuals, the thyroid enlargement is probably caused by several growth factors (including TSH):

• That act over time on thyroid follicular cells:

• That have different synthetic and growth potentials

• There is often a family history of goiter:

• Suggesting that genetic factors may also play a role

• The result is diffuse and later multinodular thyroid enlargement:

• Some nodules eventually become autonomous:

• Due to activating mutations in the TSH receptor or G proteins within the thyroid follicular cells

• The following observations support this sequence of events:

• Thyroid volume is larger in older patients

• The longer the patient has a goiter:

• The larger the size of the goiter

• The larger the size of the goiter:

• The lower the serum TSH concentration

• In patients with Graves’ disease:

• TSH receptor antibodies (TRAb):

Stimulate the TSH receptor:

• To cause thyroid growth and excessive hormonal secretion

Clinical Presentation of Patients with Goiter

  • The clinical manifestations of goiter:
    • Depends upon the presence of thyroid dysfunction and upon the growth rate of the goiter
  • Some patients may have symptoms and biochemical evidence of hypothyroidism or hyperthyroidism:
    • However, the majority of patients with goiter:
      • Are asymptomatic and biochemically euthyroid
  • Patients with longstanding, large goiters:
    • May develop symptoms of obstruction:
      • Due to progressive compression of the trachea or sudden enlargement (usually accompanied by pain):
        • Secondary to hemorrhage into a nodule
  • Asymptomatic:
    • Most goiters grow very slowly over many decades:
      • Therefore, the majority of patients with goiter:
        • Are asymptomatic
  • The goiter may first be noted on:
    • Physical examination or
    • Found incidentally on cross-sectional imaging studies performed for unrelated reasons
  • Thyroid dysfunction:
    • If the goiter is due to Hashimoto’s thyroiditis or severe iodine deficiency:
      • Patients may have symptoms of hypothyroidism:
        • For example:
          • Fatigue, constipation, cold intolerance
    • If due to multinodular goiter (with autonomy) or Graves’ disease:
      • Patients may have symptoms of hyperthyroidism:
        • For example:
          • Palpitations, dyspnea on exertion, unexplained weight loss
  • Obstructive symptoms:
    • Patients with longstanding goiters (cervical or substernal) may develop symptoms of obstruction:
      • Due to progressive compression of the trachea or sudden enlargement (usually accompanied by pain):
        • Secondary to hemorrhage into a nodule
    • The majority of patients with obstructive cervical goiters:
      • Have had a visible goiter for many years
  • Most patients with substernal goiter (77% to 90% in two series) also have visible goiters:
    • Although some are found incidentally on imaging studies performed for unrelated reasons
  • In those without visible goiter:
    • Substernal goiters may also be found:
      • Because of obstructive symptoms
  • Since goiters tend to grow slowly:
    • Substernal goiters are most commonly discovered:
      • During the fifth and sixth decades of life:
        • And are found more often in women than men
  • The most common symptom in patients with obstructive cervical or substernal goiter:
    • Is exertional dyspnea:
      • Which is present in 30% to 60% of patients:
        • This symptom usually occurs when:
          • The tracheal diameter is less than 8 mm
  • In some patients with substernal goiter:
    • Dyspnea is primarily positional or nocturnal:
      • And it occurs primarily during maneuvers that force the thyroid into the thoracic inlet:
        • Such as reaching and bending
  • When tracheal compression becomes severe (luminal diameter less than 5 mm):
    • Stridor or wheezing occurs at rest:
      • This upper airway wheezing must be distinguished from asthma
  • An upper respiratory illness:
    • May exacerbate upper airway obstruction
  • Cough:
    • Is present in 10% to 30% of patients:
      • And it may be positional
  • Pain is unusual
  • Choking sensation is common
  • Goiter may contribute to obstructive sleep apnea:
    • And thyroidectomy may improve symptoms:
      • In a study of 45 patients with snoring symptoms who were undergoing thyroidectomy for any reason (42% for goiter or compressive symptoms):
        • 29% had improved snoring frequency, apnea, and frequency of daytime somnolence after surgery
  • A variety of other symptoms can be induced by obstructive goiter:
    • Dysphagia:
      • Is a less common complaint because of the posterior position of the esophagus
  • Compression of a recurrent laryngeal nerve:
    • May cause transient or permanent vocal cord palsy:
      • Resulting in hoarseness
  • Phrenic nerve paralysis
  • Horner’s syndrome:
    • Due to compression of the cervical sympathetic chain
  • Rarely:
    • Jugular vein compression or thrombosis
    • Cerebrovascular steal syndromes
    • Even the superior vena cava syndrome

#Arrangoiz #ThyroidExpert #ThyroidSurgeon #HeadandNeckSurgeon #CancerSurgeon #SurgicalOncologist #Miami #Florida #MSMC #MountSinaiMedicalCenter #Mexico