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Diseases of the Mouth and Throat Ashley Ramos, PA-C Instructional Objectives 27. Differentiate oropharyngeal disorders by epidemiology, etiologies, risk factors, genetic influences, pathophysiology, signs/symptoms, physical examination. (CO1,CO2) 28. Distinguish oropharyngeal disorders as acute,...

Diseases of the Mouth and Throat Ashley Ramos, PA-C Instructional Objectives 27. Differentiate oropharyngeal disorders by epidemiology, etiologies, risk factors, genetic influences, pathophysiology, signs/symptoms, physical examination. (CO1,CO2) 28. Distinguish oropharyngeal disorders as acute, chronic, urgent, or emergent. (CO3, CO4) 29. Select the most appropriate clinical diagnostic tests available to classify the type of oropharyngeal disorders. (CO3) 30. Interpret the results of diagnostic tests to establish the diagnosis of oropharyngeal disorders. (CO3) 31. Apply the current and emerging pharmacologic and other non-pharmacologic evidence-based practices used in the treatment of oropharyngeal disorders. (CO4) 32. Formulate an age appropriate, comprehensive treatment plan for individual patient with oropharyngeal disorders. (CO4) 33. Identify the age appropriate health screening and health promotion/disease prevention strategies for patients with oropharyngeal disorders. (CO5) Topics to be covered Infectious/inflammatory disorders Angioedema Aphthous ulcers Candidiasis Dental abscess Dental caries Epiglottitis Gingivitis Laryngitis Peritonsillar abscess Pharyngitis Deep neck infection Salivary disorders Parotitis Sialadenitis Other oropharyngeal disorders Leukoplakia “The health status of the oral cavity is linked to cardiovascular disease, diabetes, and other systemic illnesses. Thus, examining the oral cavity for signs of disease is a key part of the physical examination (Durso, 2018).” The Mouth Oral region (the mouth) includes the following structures: Oral cavity Teeth Gingivae Tongue Palate (hard and soft) Palatine tonsils Functions of the oral region Food ingestion and beginning of digestion Chewing Forming of words Facial expression Deglutition (swallowing) The Vestibule and the Oral Cavity The vestibule is the space between the teeth/gingivae and the lips The oral cavity is considered from the inner gingiva to the roof of the mouth and the anterior 2/3rds of the tongue The mouth is bordered by the hard palate above and several muscles below; and is contiguous with the pharynx. The palate separates the oral cavity from the nasal cavities and the nasopharynx The pharynx communicates with nasal and laryngeal cavities as well Normal Variants of the oral cavity Leukoedema Fordyce granules normal variants and typically disappears if mucosa is stretched. ectopic sebaceous glands, symmetrically distributed on buccal mucosa and vermillion border. VERY COMMON Physiological oral pigmentation Oral pigmentation due to increased melanin production and can be seen in people of color; can also be seen on hard palate, buccal mucosa. Normal Tongue Variants Normal Tongue Variants Fissured Tongue: deep grooves located on the middle/evenly distributed -can also be seen in Down Syndrome -food/debris can get caught in fissures and increasing chances for developing halitosis Normal Tongue Variants Black Tongue Hyperpigmentation of the tongue and oral mucosa, commonly seen in people of color Less common causes of tongue hyperpigmentation include drugs (tetracyclines, linezolid, bismuth subsalicylate, antidepressants, proton pump inhibitors, interferon), and Addison’s disease Normal Tongue Variants Pigmented fungiform papillae: hyperpigmentation of the fungiform papillae Can be seen in people of color Usually appears in 20s-30s Tongue Abnormalities Geographic Tongue (benign migratory glossitis) Chronic Benign inflammatory condition in which there is loss of papillae leading to ulcer-like lesions on the tongue with whitish borders. Appearance can change over minutes to hours. Irregular shaped erythematous borders Fairly asymptomatic, occasionally patients have burning pain. Geographic Tongue (benign migratory glossitis) Diagnosis is clinical Central erythema due to atrophy of filiform papillae Usually no treatment needed, but if symptomatic and treatment needed: Topical steroids Anesthetic rinses Consider psoriasis if skin lesions, conjunctivitis, urethritis, arthritis, present as well Geographic Tongue: Patient should report to ER if: Tongue swells Trouble breathing Problems with eating, talking, chewing, swallowing Patient education Reassurance of benign process Avoid irritating food/drink Atrophic Glossitis Benign condition that can be caused by a variety of things including: Nutritional deficiencies (iron, vitamin B12 and folic acid) Thrush Protein-calorie malnutrition Celiac Disease Lichen Planus Sjogren’s syndrome Chemotherapy Atrophic Glossitis The tongue appears smooth, glossy, erythematous and with the loss of papillae. Patients complain of tongue soreness, burning and increased sensitivity with eating acidic food Treatment: treat the underlying condition Black Hairy Tongue A benign condition due to hypertrophy and elongation of filiform papillae The elongated filiform papillae collects debris, bacteria, fungus, etc which then causes the characteristic black pigmentation. Can be induced by antibiotics, candida and bacterial infection, poor oral hygiene, tobacco use, radiation therapy. Black Hairy Tongue Clinical presentation: Elongated filiform papillae and a yellowish white to brown/black dorsal tongue surface (posterior 2/3rds) Signs/Symptoms: alterations in taste, nausea, gagging, halitosis, pain, burning Treatment is to brush that area of the tongue with a soft-bristle toothbrush and toothpaste two to three times per day ; eating firm foods such as apples to help clean the tongue Stomatitis/ Mucositis Stomatitis: inflammation of the mouth, can be due to several etiologies. 1. Nutritional deficiencies: B12, vitamin C, folic acid, niacin 2. Chemotherapy 3. Nicotine 4. Systemic autoimmune diseases: SLE, Reiter’s syndrome, Behcet’s dz, Crohn’s disease 5. Infection: viral, bacterial, fungal Stomatitis/ Mucositis Treatment Address any suspected nutritional deficiencies or autoimmune diseases that may be uncontrolled. Encourage cessation of all tobacco. Dietary changes: avoid spicy food, acidic foods, sharp foods (chips), alcohol and alcohol containing mouthwashes. Meticulous oral hygiene Stomatitis/ Mucositis Pain Control “Magic or Miracle Mouthwash”: a compounded product- several blends. Most include a topical anesthetic (viscous lidocaine), an antacid (Maalox), diphenhydramine (to dry) +/- nystatin. Some also contain dexamethasone. Doxepin oral rinse, rinse and spit. Works by blocking histamine Benzydamine (NSAID) oral rinse Teeth and Gum Disorders Dental Anatomy Definitions Periodontal disease – diseases that affect the dental supporting structures Gingivitis- inflammation of ONLY the gums Periodontitis – gingival inflammation PLUS loss of supportive connective tissues Gingivitis/Periodontitis Gingivitis is the most common form of periodontal disease Periodontitis is a major cause of tooth loss GLOBALLY Most US adults have slight to moderate periodontitis 5-15% have server Gingivitis/Periodontitis Etiology Most commonly caused by a bacterial biofilm (plaque) Other causes peri-implant disease necrotizing periodontal disease pregnancy gingivitis linear gingival erythema vitamin C deficiency drug-induced gingival overgrowth gingival recession abscesses Gingivitis/Periodontitis: Clinical Presentation Gingival redness Swelling Bleeding that is provoked by routine brushing or flossing Increased probing depth (periodontitis) Increased tooth mobility (periodontitis) Gingivitis/Periodontitis: Physical Exam/Dx Gingival redness Swelling Easy bleeding when provoked Halitosis Increased probing depth (periodontitis) Increased tooth mobility (periodontitis) Clinical diagnosis Dental referral (debridement for periodontitis) Prevention Gingivitis/Periodontitis: Treatment/Prevention Regular brushing with toothpaste and flossing Antimicrobial/antiseptic mouth wash Regular dental exams Dental Caries (Cavities/Tooth Decay) Permanently damaged areas in teeth that develop into tiny holes 1 in 4 adults aged 20-64 and 1 in 6 > 65 years old Male > female Etiologies vary with age Important contributor to tooth loss S. mutans Dental Caries (Cavities/Tooth Decay): Risk Factors Poor oral hygiene Ingestion of carbohydrates Smoking Dental Caries (Cavities/Tooth Decay): Pathophys Bacteria ferments using dietary sugar and produces acids that lower the pH on tooth surface and cause enamel and dentin destruction Natural tooth protections: Constant flow of saliva Cleansing action of the tongue Acquired pellicle Dental Caries (Cavities/Tooth Decay): Physical Exam Physical exam Pits and fissures on affected tooth surface (early) Stains and collapse of enamel, pain, tooth sensitivity (late) Biodigital Dental Cavities Treatment Restorative therapy (fillings) Prevention Fluoride (water supply, toothpaste) Brushing teeth 2x daily Flossing after each meal Reduction of sugar rich foods Smoking cessation Regular dental visits Dental Abscess Pocket of pus caused by a bacterial infection Periapical Periodontal Lower third molar most common Dental Abscess: Risk Factors Poor dental hygiene Deep periodontal pockets Incomplete removal of subgingival calculus Occlusion of the pocket orifice by foreign bodies (ie, popcorn kernel) Inadequate treatment of periodontitis Poorly controlled diabetes High sugar diet Xerostomia Dental Abscess: Presentation Asymptomatic Painful swelling of the buccal or lingual/palatal gingiva Fever Painful tooth/teeth in the affected region, Discomfort with chewing Tender/swollen lymph nodes Halitosis Swelling of the face/cheek Thermal sensitivity Dental Abscess: Physical Exam Findings Gingiva Swelling Warmth erythema Fluctuant mass Tenderness to palpation Increased tooth mobility Enlarged and tender lymph nodes Neck/face swelling Dental Abscess: Diagnosis Uncomplicated Clinical Complicated CBC CMP Blood cx Lateral and a/p neck xrays Head and neck CT Dental Abscess: Treatment and Complications Treatment Dental/HEENT referral I&D --> abx (Amoxicillin 500mg PO x1, then 500mg PO q 8hsr x 3 days OR Clinda for PCN allergic) Pain control Complications Sepsis Osteomyelitis of the head/jaw bones Fistula Soft tissue infection Infectious and Inflammatory Disorders Oral Candidiasis (Thrush) Oral Candidiasis (Thrush) Infection of the buccal mucosa by Candida species, most commonly C. albicans Commonly seen certain populations: infants and neonates (1-6 months) patients on antibiotics or steroids (oral or inhaled) patients with endocrine disorders underlying immune dysfunction: may be the first sign of HIV Denture wearers with poor oral hygiene Thrush Pathophysiology Overgrowth of yeast on the oral mucosa leads to abnormal shedding of epithelial cells and accumulation of bacteria, keratin, and necrotic tissue into a pseudo membrane, which may closely adhere to the mucosa. Thrush: Patient Presentation Asymptomatic Oral pain Throat pain Difficulty swallowing Burning with chewing Loss of taste Thrush: Physical Exam Findings White plaques that CAN be scraped off Buccal, palate, tongue and/or the oropharynx Erythematous gingiva without plaques (atrophic form/denture stomatitis) Thrush: Diagnosis Clinical diagnosis Scraping w/tongue depressor and KOH prep Budding yeasts +/- hyphae Mild, moderate, severe disease Culture HIV testing Thrush Treatment Mild disease topical therapy x 7-14 days Clotrimazole troches – 10 mg five times daily Miconazole buccal tablets – 50mg once daily Nystatin rinse QID Systemic therapy Fluconazole Moderate – severe disease Fluconazole- 200mg loading dose followed by 100-200mg daily Other azole and amphotericin B alternative options Aphthous ulcer Aphthous Ulcers (Ulcerative stomatitis) The most common form of ulceration in the oral cavity. Also known as “canker sores” Etiology unknown Very common- affecting slightly more women than men Typically lasts 7-14 days, but may be recurrent May be single or multiple. Usually less than 5 mm in size and heal without scarring. Aphthous Stomatitis/ Ulcers: Etiology Since there is no microorganism associated with recurrent aphthous stomatitis (RAS), it is not infectious, contagious, or sexually transmitted. Aphthous Ulcers (Ulcerative stomatitis): Risk Factors Parent with h/o Female Non smokers High level of stress Elevated socioeconomic status Neutropenia of any kind Oral trauma NSAIDS, ACEi, Beta blockers Food and chemical sensitivities Nutritional Deficiencies Aphthous Stomatitis/ Ulcers: Associated Common Diseases Systemic diseases associated with aphthous ulcers include: HIV- r/o opportunistic pathogens, bx, HAART Behҫet syndrome: recurrent oral and genital ulcers Celiac disease: gluten sensitivity Systemic lupus: an autoimmune condition Inflammatory bowel disease: Crohn’s, ulcerative colitis, autoimmune conditions Neutropenia for any cause Aphthous Ulcers (Ulcerative stomatitis) Clinical Presentation PAINFUL, afebrile Single or multiple small, red, round/oval spots with a prodromal tingling/burning that can occur 1-2 days before the ulcer. The ulcer is clearly defined, shallow, round, or oval with a red halo and a yellowish-gray center. Pain usually dissipates after 3-4 days and the lesion turns gray, at which point epithelialization occurs. Total resolution 7-10 days Aphthous Ulcers (Ulcerative stomatitis) Diagnosis Clinical diagnosis Biopsy CBC E sed rate C-reactive protein Vit B12, folate, iron, Vit D Aphthous Stomatitis/ Ulcers Treatment Oral hygiene Soft toothbrush, non EtOH mouthwash Avoid exacerbating factors spicy foods, citrus, hot foods, smoking and EtOH Pain control (topical analgesic) Viscous lidocaine/benzocaine Control secondary infection Topical corticosteroids 1st line – high potency Dexamethasone elixir 0.5mg/5ml TID-QID Clobetasol 0.05% gel or ointment TID Aphthous Stomatitis/ Ulcers Treatment Severe RAS: Oral steroids Montelukast Colchicine Pentoxifylline Dapsone Clofazimine Thalidomide Vitamin C reduces the frequency of minor RAS and severity of pain Aphthous Stomatitis/ Ulcers Treatment Nonna’s cure: Wet finger, dip in salt, place directly over apthous ulcer. It hurts to do this but sort of “cauterizes” the ulcer, gets the pain to resolve, and gets the ulcer to go away majority of the time. Recurrent episodes or prolonged ulcer should prompt CBC, ESR, serum iron studies, B6, B12, folate levels, as well as biopsy of the affected tissue. Cheilitis Cheilitis An acute or chronic inflammation of the lips. Usually involves the lip vermilion and the vermilion border, but the surrounding skin and the oral mucosa may also be affected. Common symptoms include erythema, dryness, scaling, fissuring, edema, itching, and burning. Cheilitis Types Eczematous Irritant contact Allergic contact Atopic Actinic (solar) – premalignant Angular Cheilitis Presentation/Diagnosis Examples of: Angular cheilitis (A) erythema and fissures at corners of the mouth Clinical diagnosis/KOH prep A B Actinic (B) – diffuse atrophic changes with erosion Clinical diagnosis/biopsy Allergic cheilitis (C/D) with scaling and erythema Clinical diagnosis/biopsy C D Treatment of Cheilitis Irritant, allergic, and atopic cheilitis Mainstay of treatment: discontinue/remove causative irritant or allergen from the patient’s environment Angular cheilitis treatment of infection of candida or less commonly, s. aureus. Actinic cheilitis Cryotherapy, 5-FU, CO2 laser ablation Pharyngitis Pharyngitis/ Tonsillitis Inflammation of the pharynx due to an infection or irritation Most common etiology is infectious. Other causes include trauma, toxins, allergy and neoplasm. The most common infectious cause is viral (rhinovirus, adenovirus, influenza, EBV, coxsackievirus) Most bacterial cases are caused by group A streptococci (GAS) (Strep pyogenes). Infectious Pharyngitis/ Tonsillitis US children experience an average of 5 URIs per year, and one Group A Strep (GAS) infection every 4 yrs. US adults experience 2-3 URIs per year and one GAS infection every 8 years on average. GAS pharyngitis is most common through winter to early spring. Infectious Pharyngitis/ Tonsillitis General pathophysiology Virus or bacteria directly invade the pharyngeal tissues causing inflammation. Pharyngitis/tonsillitis: Risk Factors History of URI Known exposure to Group A Strep Immunodeficiency Chronic irritation Smoking Allergies Acid reflux THROAT” Tonsillitis: Signs and Symptoms Pharyngitis/ “SORE Rhinorrhea Cough Congestion Oral ulcers Hoarseness Odynophagia Fever Lymphadenopathy Fatigue Infectious Pharyngitis/ Tonsillitis How do we determine if viral or bacterial? Bacterial History More common in kids 4-7 years More likely to be sudden onset Fever Sick contacts with GAS increase the likelihood Viral History Sub-acute onset: More likely if patient has had coughing or rhinorrhea for several days Associated with cough Hoarseness Coryza Myalgias Infectious Pharyngitis/ Tonsillitis How do we determine if viral or bacterial? Bacterial Exam Petechiae of the pharynx or palate (may also be seen in mono) Anterior cervical LAD Tonsillar exudates more likely Strawberry tongue Rash No cough Fever Viral Exam Cough Conjunctivitis Rhinorrhea Infectious Pharyngitis/ Tonsillitis How do we determine if viral or bacterial? What symptoms and signs are not reliable in differentiating viral from bacterial etiology? Fever or lack of fever Tonsillar or pharyngeal exudates Petechiae Exudates Pharyngitis/ Tonsillitis: Centor Criteria Centor criteria of 0-1pt: Low chance of GAS cause Centor criteria of 2-3 pt: Moderate risk Centor criteria of 4 pt: High risk GAS bacterial pharyngitis Strep Pharyngitis Centor Score Calculator (mdapp.co) Point systems for Group A Strep Pharyngitis Fever or temperature of 38°C (100.4°F) (1 point) Absence of cough (1 point) Tender anterior cervical lymph nodes (1 point) Tonsillar swelling or exudates (1 point) <5 years (1 point) 5 to 15 years (0 points) >15 years (-1 point) Pharyngitis/ Tonsillitis: Making the Dx Viral – clinical diagnosis Bacterial Throat culture (gold standard): 90-99% sensitive and specific Less expensive but multiple days to result Rapid antigen detection testing (RADT) 95% sensitive, and 98% specific. If peds patient has symptoms and negative rapid, cx is recommended Strep Pharyngitis: Differential Dx Respiratory viruses Other bacteria: Neisseria gonorrhoeae, Mycoplasma and Chlamydia trachomatis What not to miss: HIV: early seroconversion Mononucleosis (EBV): larger and more extensive cervical LAD, splenomegaly Diptheria: grey pseudomembrane that bleeds upon removal, ill, low grade fever Differentials Diptheria Thursh Pharyngitis/ Tonsillitis Management Viral Symptomatic tx GAS Symptomatic Antibiotics Abx helps to prevent complications such as: otitis media, sinusitis, peritonsillar abscess and rheumatic fever Pharyngitis/ Tonsillitis: Empiric ABX Penicillin is the first line therapy of GAS Adults/teens: Pen VK 500 mg po bid OR amoxicillin 500mg BID or 1g daily x 10 days PCN allergic: cephalexin, cefadroxil, clindamycin, azithromycin, clarithromycin Children: Pen VK 250mg po bid-tid x 10 days in children OR Amoxicillin 50mg/kg q day for 10 days If needed, Amoxicillin can be broken up into 25mg/kg/day q 12 hours Amoxicillin suspension may be used in young children due to it’s better taste. Pharyngitis/ Tonsillitis: Patient ed When can they return to work/school? CDC recommendation is once on abx for 24 hours they are safe to return to school/work. If still febrile the patient can request an extension Follow up if worsening (ie swallowing and breathing difficult) Recurrent GAS pharyngitis will likely need tonsillectomy Explain viral vs bacterial Complications of bacterial Strep Complications Scarlet Fever/ Scarlatina Develops in less than 10% of all cases of “strep throat”. Characterized as strep throat PLUS rash May follow a streptococcal wound infection, burns, but most cases are associated with pharyngitis/ tonsillitis. A toxin produced by the streptococcus causes the pathognomonic rash as well as other s/s. More intense rash with reddened flexor creases and facial flushing with circumoral pallor. spares hands and feet Scarlet Fever/ Scarlatina Rash Rash usually appears 12-48 hours after fever onset and lasts 4-5 days Fine desquamation (flaking of the affected skin) occurs in 7-10 days Scarlet Fever/ Scarlatina Rash Diffuse erythema, red papules. “sunburn with goose bumps” Orange-red punctate lesions with a coarse sandpaper texture. Initially rash occurs on neck/chest/ axillae then spreading to abdomen and extremities. Rash blanches with pressure, may be pruritic, but usually not painful. Scarlet Fever/ Scarlatina: other S/S Strawberry tongue: initially white strawberry tongue: a white coating with prominent red papillae. By the 4th-5th day the white membrane sloughs and the tongue appears shiny and red Fever: up to 103-104 Abdominal pain: may mimic acute abdomen Scarlet Fever: Diagnosis/ Management Clinical diagnosis Need to find source of infection Treatment is same as strep throat Scarlet fever is highly contagious- wash hands, quarantine the afflicted! Rash may be treated symptomatically with emollients. Streptococcal Glomerulonephritis Usually occurs 7-12 days after strep pharyngitis or other strep infection (impetigo) Common manifestations for all glomerulonephritis: Urinary: oliguria (develops as GFR decreases) ,anuria, hematuria, proteinuria Edema: face, eyes, arms, feet and ankles (due to NA and water retention) Hypertension Abdominal pain Back pain Glomerulonephritis: S/s, labs. dx o o o o Elevated antistreptococcal antibody (ASO) titer Decreased GFR Elevated serum creatine UA with proteinuria, hematuria o Dx: clinical o Signs of acute nephritis PLUS confirmed recent GAS infection Other post strep complications to be aware of Streptococcal toxic shock syndrome: rare complication. Causes shock and organ failure Post streptococcal reactive arthritis: arthritis involving one or more joints AFTER infection Pediatric autoimmune neuropsychiatric disorder associated with group A strep (PANDAS): subset of kids whose OCD or tic symptoms are worsened by GAS infection Tonsillopharygneal cellulitis/abscess Otitis media Sinusitis Meningitis Juglar vein septic thrombophlebitis Laryngeal Disorders Laryngeal Disorders Laryngeal Disorders The primary symptoms of these disorders are hoarseness and stridor. “Breathy” voice: air passing over vocal cords that are incompletely opposed Hoarseness: air turbulence created by irregular vocal cords Stridor: a high pitched whistling produced from a narrowed airway. https://www.youtube.com/watch?v=oeoAze-CHng Laryngitis Laryngitis Inflammation of the larynx causing hoarseness Acute < 3 weeks Chronic > 3 weeks Laryngitis: Etiology Acute URI Acute vocal strain Chronic Irritants Laryngopharyngeal reflux Muscle tension dysphonia Vocal cord lesions (benign or malignant) Laryngitis: Clinical Presentation/Physical Exam HOARSENESS! No pain Physical exam Hoarseness (need descriptors) Examine ears, upper airway, oral cavity, CN function and respiration If patient complaint is for >2 weeks in absence of history of URI --> ENT referral for full exam with visualization of the laryngopharynx Laryngitis: Treatment Acute Supportive care Rest your voice; avoid talking, don’t whisper Treat body well: Eat well, rest, gentle exercise, lots of water, hot tea Systemic glucocorticoids Chronic Remove offending agent Treat underlying cause Epiglottitis Epiglottitis (supraglottitis) Inflammation of the supraglottic area, epiglottis, and pharyngeal structures Can be life threatening Pediatric population, 2-7 years old (peak 3-5 years of age) Very acute Caused by H. influenzae type B S. Pneumoniae S. pyogenes Epiglottitis: clinical presentation Young children: Abrupt onset and rapid progression of: respiratory Distress Dysphagia Drooling Muffled voice High fever Respiratory retractions Adults: similar sxs but more gradual onset Epiglottitis: Physical Exam Ill appearing Low pitched stridor Anxious Tripod posture a sitting position, leaning forward, neck hyperextended, and chin thrust forward direct exam in any patient with epiglottitis may provoke sudden airway closure due to laryngospasm Epiglottitis: Imaging/Labs Lateral neck xray Swollen epiglottis (thumbprint sign) Thickened aryepiglottic folds Obliteration of the epiglottic depression at the base of the tongue Fiber optic examination Used to confirm diagnosis Completed with anesthesia and HEENT Cherry red and swollen epiglottis Throat cx + H. flu type B Epiglottitis: Treatment 1. 2. 3. 4. 5. 6. Airway management!!! Supplemental humidified oxygen and monitor ENT consult IV Antibiotics: usually a third gen cephalosporin (ceftriaxone) and vancomycin for MRSA coverage IV corticosteroids Monitoring in the ICU setting +/- bronchodilators, racemic epinephrine (differing opinions) Deep Neck Infections Anatomy Review 3 layers of deep cervical fascia Superficial (Investing) Middle (Pretracheal) Deep (prevertebral) Deep Neck Infections: General Features/Complications Symptoms Complications Severe neck/throat pain Carotid sheath involvement Neck/throat swelling Extension into mediastinum Fever Spinal epidural abscess Systemic toxicity Cervical osteomyelitis Deep Neck Infections: General Diagnosis/Treatment Diagnosis Xray CT MRI Culture Treatment Airway management Abx I&D Peritonsillar Abscess and Cellulitis Peritonsillar cellulitis vs abscess PT cellulitis: inflammation of the space between the palatine tonsil capsule and the pharyngeal muscles Caused by infection but no pus PT abscess (quinsy): inflammation of same space WITH pus Often polymicrobial infection GAS, MSSA/MRSA and respiratory anaerobes PTA: Epidemiology Most common deep neck infection Affects adolescents and young adults ~14 per 100,000 Peritonsillar Abscess: Risk Factors H/o GAS infection Smoking Periodontal disease Chronic tonsillitis Immunocompromised Peritonsillar Abscess (PTA): presentation Vocal changes Drooling Difficulty swallowing (Odynophagia) Painful swallowing (Dysphagia) Limited oral extension Severe sore throat Peritonsillar Abscess (PTA): Physical Exam Ill appearing Fever Malaise Displaced uvula to contralateral side Cervical LAD Trismus (difficulty opening the mouth) Drooling Muffled voice “hot potato voice” Displacement of affected tonsil Deviation of soft palate and asymmetric rise of uvula are very PTA: Physical Exam PTA: Dx Clinical Diagnosis CBC BMP Blood cultures Throat Culture Rapid strep CT scan soft tissue neck with IV contrast Needle aspiration and cultures Group A Strep PTA: DDx Tonsillitis Epiglottitis Peritonsillar cellulitis Infectious mononucleosis Retropharyngeal abscess Neoplasm Internal carotid artery aneurysm PTA: Tx Needle aspiration…Done by ENT or EM doc or you in rurual settings Consider your anatomy and location of carotid when this is done Diagnostic Therapeutic for 90% of PTAs Need to consider Airway management Following adequate needle aspiration or I&D, antibiotic therapy is recommended should cover Gram post and anaerobes Tonsillectomy is no response in 24 hrs of treatment PTA: Tx ICU Hydration ENT consult Initial abx Non-toxic appearing patient IV Ampicillin-sulbactam (Unasyn) or Clindamycin Moderate to severe or do not respond to above Add IV vanco or linezolid After improvement PO Amoxicillin-clavulante or Clindamycin +/- Vanco Total course of abx should be 14 days PTA: Complications Septic jugular vein thrombophlebitis Airway obstruction and aspiration Carotid artery rupture or pseudoaneurysm Bacteremia/ sepsis Lemierre Syndrome Most patients fully recover without complications Retropharyngeal Abscess VH Dissector Link Retropharyngeal Abscess (RPA) Abscess located in the tissues in the back of the throat behind the posterior pharyngeal wall. Anterior to the prevertebral fascia Can extend from base of skull to tracheal bifurcation Usually polymicrobial Most common are: GAS, S.aureus and Bacteroides Retropharyngeal Abscess: Epidemiology/Etiology / Risk Factors Common in children < 5 years of age trauma foreign bodies such as a fishbone Intraoral procedures Extension from dental infection or Ludwig angina Recent ear, throat, sinus infection Immunocompromised RTA Pathophys • the retropharyngeal space contains lymph nodes that drain the nasal cavity, paranasal sinuses, nasopharynx, oropharynx, and hypopharynx • infections involving these structures can lead to a lymphadenitis, which may progress to the formation of a retropharyngeal abscess Retropharyngeal Abscess: Clinical Presentation Sore throat Fever Dysphagia/odynophagia Torticollis (stiff neck) stridor Trismus poor oral intake muffled voice “hot potato voice” respiratory distress Retropharyngeal Abscess: Physical Exam Fever Dysphagia/odynophagia Torticollis stridor Trismus cervical lymphadenopathy muffled voice “hot potato voice” respiratory distress Midline or unilateral swelling or bulging of posterior pharyngeal wall Retropharyngeal Abscess: Diagnosis and Treatment Diagnosis CT scan neck with IV contrast (gold standard) Loss of definition between anatomic spaces in the neck Treatment Immediate consult from ENT specialist for surgical intervention (I &D) Airway management Stranding in the subq tissues IV hydration Tissue enhancement IV antibiotics Frank abscess formatin Unasyn IV or CBC Ceftriaxone or levo PLUS BMP Flagyl or Clinda IV Blood cx Piperacillin-tazobactam Retropharyngeal Abscess: Ddx Retropharyngeal space tumor Foreign body Aneurysm Hematoma Lymphadenopathy Variable Epiglottitis Retropharyngeal Abscess Peritonsillar Abscess Age Group 3-7 years peak (but can affect adults) 6m-6 years, but can affect adults Usually >10 Pathogen H. influenzae Usually microbial, GAS most GAS common H&PE Sudden Resp distress, toxic appearance, acute decompensation, drooling, inspiratory stridor Sore throat, trismus, “hot potato” voice, drooling, cervical LAD Sore throat, “hot potato voice”, trismus, drooling, uvula displacement to unaffected side Fever YES, HIGH YES, HIGH potentially Position preferred Tripod Supine with extended neck n/a Imaging Findings CXR- “thumb sign” CT scan with decreased planes Usually clinical diagnosis Treatment Abx, intubation (possibly), IV hydration I&D, abx I&D, abx, tonsillectomy (possibly) Ludwig’s Angina Bilateral infection of the submandibular, sublingual, and submental spaces that begins in the floor of the mouth, most commonly related to the second or third mandibular molar teeth. Polymicrobial Risk Factures: Diabetics IV drug use Dental infection (2/3rd of cases) Ludwig’s Angina: Clinical presentation Trismus, dysphagia and odynophagia Fever Drooling Stiff neck Muffled “hot potato” voice Poor dental hygiene Stridor Cyanosis Ludwig’s Angina: Clinical presentation Tender, symmetric, and "woody" induration Lingual swelling NO LAD Elevated oral cavity, tender, and erythematous Trismus, dysphagia and odynophagia Fever Drooling Stiff neck Muffled voice Poor dental hygiene Ludwig’s Angina: Diagnosis Clinical diagnosis CT of neck w/ IV contrast soft tissue thickening increased attenuation of the subcutaneous fat loss of fat planes in the submandibular space gas bubbles within soft tissues (“bubble sign”) focal fluid collections muscle edema MRI Neck ultrasound CBC CMP Blood cx Ludwig’s Angina: Treatment All patient require emergent consult from an ENT specialist Initial management should focus on providing a definitive airway Awake fiber optic intubation Tracheostomy IV hydration and IV antibiotics IV Unasyn or Ceftriaxone +/- Vanco Levo PCN allergic May take more than a week for edema to resolve with ATB therefore airway management is needed Diseases of the salivary glands Quick Definitions Xerostomia: mouth dryness due to decrease saliva production that can be causes by medications, diseases, radiation etc Sialorrhea: increased saliva production and be caused by a variety of conditions including pregnancy and acute inflammation of the oral cavity Sialolithiasis: calcified stones that are in the salivary gland ducts Parotitis: inflammation of the parotid gland Sialadenitis: inflammation of any salivary gland (can be acute or chronic) Disease of the Salivary Glands The salivary system contains 2 parotid glands, 2 submandibular glands, 2 sublingual glands and hundreds of minor salivary glands. These glands and their associated ducts can get infected and/or blocked causing swelling, pain, and xerostomia Sialolithiasis Calculi are more common in the submandibular glandWharton’s duct (80-90%) than Parotid Gland- Stenson’s duct (6%-20%) or the minor salivary ducts (1-2%) Stones are relatively common (1% of autopsies) but usually clinically silent. 75% are single stones. Most common in men, aged 30-60 years. Sialolithiasis Pathophysiology Pathophysiology is unknown, but is thought to be precipitation of calcium during salivary stasis, especially with glandular inflammation. Risk factors include: Dehydration Medications (diuretics and anti-cholinergics) Trauma to the gland Smoking Gout-uric acid crystals precipitate out of solution Sialolithiasis Presentation Symptoms may include Pain and swelling over the affected gland before or during eating. Generally a waxing/waning pain. Repeated bouts of sialadenitis On exam, it may be possible to feel the stone or to “milk” it from the duct to appear Duct/gland may be tender, particularly if concurrent sialadenitis is present. Sialolithiasis Dx Clinical diagnosis History and physical exam are mainstays Sudden onset of swelling and pain of gland Worse with eating/preparing to eat Tenderness of duct on exam Decreased saliva production Stone on exam High resolution, non-contrast CT scan of the facial bones is the diagnostic study of choice (most stones contain enough calcium to be seen without contrast). Sialolithiasis Tx moist heat sialogogues (saliva production) good hydration milking the duct NSAIDs are given for pain with prn opioids If the stone is not removed with these conservative measures, a procedural approach is undertaken by otolaryngology. Lithotripsy, wire basket retrieval using endoscopy or fluoroscopy, surgery Milking the duct (975) Really BIG Salivary Gland Stones – YouTube (975) Sialendoscopy -- Minimally Invasive Treatment of Salivary Stones – YouTube (975) Wharton's Duct Sialolith Removal - YouTube Sialadenitis Acute = swelling/symptoms < 3-4 weeks Chronic > 4 weeks Most common causes: Obstruction Bacterial infection Typically presents unilaterally Obstructive Sialadenitis: Presentation Enlarged tender gland WITHOUT the overlaying skin erythema and warmth Swelling occurs within secs to minutes of salivary production (eating, smelling food) Patient is afebrile Obstructive Sialadenitis: Physical exam/Treatment Tenderness of gland Obvious stone Decreased saliva production/mucous like output when massaging the duct Treatment: same as sialolithiasis + stopping meds that decrease saliva production Imaging if no resolution CT scan (high sensitivity for stones) Ultrasound Magnetic resonance sialography Conventional sialography (not used as much) Bacterial Sialadenitis (suppurative sialadenitis): Pathophysiology Pathophysiology: most commonly caused by stasis of saliva in the duct, resulting in ascending spread of oral flora to the gland. What facilitates this? Obstruction: stone, mass, or lesion Decreased saliva production, will decrease flow: Sjogren’s syndrome, sicca complex Hyper-viscosity of saliva: Medications like 1st gen antihistamine, diuretics, drugs with anticholinergic effects Overgrowth of bacteria: poor oral hygiene Bacterial Sialadenitis Pathophys Infection is generally polymicrobial and includes gram positive organisms and anaerobes. Most common pathogen is Staph aureus If the patient is hospitalized when sialadenitis develops, gram negative organisms may be seen. Enterobacter, Klebsiella in diabetics Bacterial Sialadenitis (suppurative sialadenitis): Presentation Usually affects the parotid or submandibular glands unilaterally. Typical s/s include: 1. Abrupt onset of unilateral swelling and firmness of the gland 2. Exquisite localized pain 3. Dysphagia or trismus 4. Systemic symptoms of infection (fever, chills, elevated WBC) Bacterial Sialadenitis (suppurative sialadenitis): Physical Exam Exam findings may reveal: Induration Edema Duct purulent drainage (sometimes requires massage of the gland) Extreme localized tenderness Bacterial Sialadenitis (suppurative sialadenitis): Physical Exam Bacterial Sialadenitis (suppurative sialadenitis): Diagnostic Work-up Diagnosis is suspected by clinical grounds U/S is a fair choice to detect stones as the cause of sialadenitis, can detect abscess CT scan of the head and neck with IV contrast is best to differentiate abscess from cellulitis Elevated serum amylase level in the absence of pancreatitis CBC Bacterial Sialadenitis Treatment Treatment includes INPATIENT ADMISSION for IV hydration, IV ABX to avoid deep tissue infection. Frank abscess will require an I&D. Antibiotic regimen should be empiric and cover the typical microbes Immunocompetent Patients: Ampicillin-sulbactam 3g IV q 6 hours OR Ceftriaxone 1g q 24 hours PLUS Metronidazole 500 mg IV q 8 hrs ABX are continued for 10-14 days, but may be converted to oral when the patient clinically improves. Bacterial Sialadenitis Treatment Immunocompromised Patients or Hospital acquired infection: Vancomycin and one of the following Metronidazole 500mg IV q 8 hrs + cefepime 2g IV q 12 hrs imipenem 500mg IV q 6 hours meropenem 1g IV q 6 hours piperacillin-tazobactam 4.5 g IV q 6 hours Bacterial Sialadenitis: Complications Massive swelling of the neck resulting in airway obstruction Osteomyelitis of the facial bones Septic phlebitis of the jugular vein Sepsis Facial nerve palsy Skin Fistulas Copyrights apply Copyrights apply Copyrights apply Copyrights apply Copyrights apply Oropharyngeal Neoplasms Leukoplakia –Epidemiology Defined as “white plaques of questionable risk” Pre-malignant Occurs in 0.5-2.0% of adults Due to changes of the epithelium at the molecular level causing dysplasia Entire pathogenesis widely unknown Leukoplakia: Risk Factors Smoking Alcohol use Tobacco Chewing HPV infection Trauma to oral cavity Oral chemical/carcinogen exposure Leukoplakia: Patient presentation Usually painless New “white” spot in mouth Does not scrape off Can present as homogenous vs nonhomogenus Leukoplakia Clinical features with increased risk of oral cancer Nonhomogeneous clinical subtype large size (>4 cm in largest diameter) extension over more than one anatomical site localization (lateral border of the tongue and floor of the mouth) Leukoplakia: Diagnosis Biopsy Benign hyperkeratosis (not reactive) Parakeratosis Atrophy Inflammation Hyperplasia, including atypical verrucous hyperplasia (not reactive), without dysplasia Various grades of dysplasia (mild, moderate, severe, or alternatively defined as low or high grade) Surgery for excision and to confirm presence of malignancy Leukoplakia: Treatment May recur after excision Decrease risk factors Surveillance at regular intervals HEENT referral Oral hairy leukoplakia White lesion that can be found on the tongue. Typically a result of Epstein Barr Viral infection and HIV/AIDS manifestation Affects the lateral portion of the tongue, floor of the mouth, palate, buccal mucosa Described as “corrugated PAINLESS” plaques Does not scrape off on physical exam Treatment: antivirals Premalignant Lesions: Erythroplakia Term is reserved for red lesion in the oral mucosa. "fiery red patch that cannot be characterized clinically or pathologically as any other definable disease." It requires a biopsy to rule out dysplasia, majority will progress to malignancy (90% will be either dysplastic or malignant) Presents as a distinct flat or slightly depressed red lesion with a smooth or granular surface Malignancies Head and Neck Malignancies Clinical presentation is representative of site of primary tumor Need bx to confirm diagnosis HPV Oropharyngeal Malignancies Affects any area of the oropharyngeal cavity 48 K new cases each year More common in males vs female Usually diagnosed after the age of 55; median age is 62 More common in Caucasian male Oropharyngeal Malignancies Risk Factors Tobacco use Alcohol use HPV infection Immunosuppression Excess sun exposure (cancers of the lips) Oropharyngeal Malignancies Clinical Presentation Leukoplakia/erythroplakia (early cancer) Induration Persistent ulceration Tissue proliferation Tissues erosion Oropharyngeal pain/paresthesia Oropharyngeal Malignancies Distribution Tongue Floor of mouth Lower lip vermilion Lateral tongue, soft palate, tonsils (HPV related) Oropharyngeal Malignancies Ddx Benign conditions Pharyngitis Tonsilitis Laryngitis Oropharyngeal Malignancies Diagnosis and Treatment BIOPSY! Referral to ENT if you are not comfortable doing bx Referral to ENT/ENT-oncology for treatment Surgical excision, chemotherapy, radiation STOP SMOKING AND ETOH use IMMEDIATELY Sources Jameson, J. L., Fauci, A. S., Kasper, D. L., Hauser, S. L., Longo, D. L., & Loscalzo, J. (2022). Harrison’s principles of internal medicine (21st ed.). McGraw-Hill Education. Norris, T. L. (2019). Porth’s essentials of pathophysiology (5th ed.). Wolters Kluwer. Chow, A. W. (2021, July 2). Submandibular space infections. UpToDate. https://www.uptodate.com/contents/submandibular-space-infections-ludwig-angina?search=ludwigs%20angina&source =search_result&selectedTitle=1~9&usage_type=default&display_rank=1 Chow, A.W. (2020, July 13). Deep neck space infections in adults. UpToDate. https://www.uptodate.com/contents/deep-neck-space-infections-in-adults?search=retropharyngeal%20abscess&source =graphics_search&graphicRef=51505 Woods, C.R. (2021, Sep 8). Epiglottitis (supraglottitis): clinical features and diagnosis. UpToDate. https://www.uptodate.com/contents/epiglottitis-supraglottitis-clinical-features-and-diagnosis?search=epiglottitis&source= search_result&selectedTitle=1~41&usage_type=default&display_rank=1 Wald, E.R. (2022, March 11). Peritonsillar cellulitis and abscess. UpToDate. https://www.uptodate.com/contents/peritonsillar-cellulitis-and-abscess?search=peritonsillar%20abscess&source=graphics _search&graphicRef=69943 Pichichero, M.E. (2021, January 15). Complications of streptococcal tonsillopharyngitis. UpToDate. https://www.uptodate.com/contents/complications-of-streptococcal-tonsillopharyngitis?search=strawberry%20tongue&s ource=graphics_search&graphicRef=68321 Usatine, R. P., Smith, M. A., Mayeaux, E. J., & Chumley, H. S. (2018). The color atlas and synopsis of family medicine (3rd ed.). McGraw-Hill Education Sources Kauffman, C. (2023 Jun 26). Oropharyngeal candidiasis in adults. UptoDate. https://www.uptodate.com/contents/oropharyngeal-candidiasis-in-adults?search=thrush&source=search_result&selectedTitle=1~150&usage_type=defa ult&display_rank=1#H2902787605 Brice, S. (2023 Aug 02). Recurrent aphthous stomatitis. Uptodate. https://www.uptodate.com/contents/recurrent-aphthous-stomatitis?search=aphthous%20ulcers&topicRef=5572&source=see_link#H1733884228 Lodi, G. (2023 Nov 20). Oral leukoplakia. Uptodate. https://www.uptodate.com/contents/oral-leukoplakia?search=leukoplakia&source=search_result&selectedTitle=1~57&usage_type=default&display_ran k=1#H3782431165 Chow, A. (2022, Oct 4). Ludwig Angina. Uptodate. https://www.uptodate.com/contents/ludwig-angina?search=peritonsillar%20abscess&topicRef=3415&source=see_link#H975545656 Chow, A. (2023 Nov 28). Epidemiology, pathogenesis, and clinical manifestations of odontogenic infections. Uptodate. https://www.uptodate.com/contents/epidemiology-pathogenesis-and-clinical-manifestations-of-odontogenic-infections?search=dental%20carie s&source=search_result&selectedTitle=3~139&usage_type=default&display_rank=3#H14 Neck Trauma Neck Trauma •The neck contains a high concentration of vascular, airway, digestive and spinal structures •Patients with injuries to the neck: • May demonstrate signs of shock: • Altered mental status, diaphoresis, tachycardia and hypotension •Patients should be placed and kept in a hard cervical collar (c-spine precautions) Neck Trauma •There are 3 main fascial layers of the neck • Platysma (investing) • Pretracheal & retropharyngeal layers • Prevertebral (tight fascial compartments) •The neck anatomy is divided into: • Anterior & posterior triangles • 3 Zones Posterior Triangle Triangles of the Neck • Middle third of the clavicle • Anterior border of the trapezius muscle • Posterior border of the sternocleidomastoid muscle Anterior Triangle • Anterior midline of neck • Lower border of the mandible • Anterior border of the sternocleidomastoid muscle Posterior Triangle of the Neck Anterior Triangle of the Neck Triangles of the Neck Anterior Triangle • Carotid artery • Internal jugular vein • Vagus nerve • Thyroid gland • Larynx • Trachea • Esophagus Posterior Triangle • Fewer vital structures • At the base of the posterior triangle • Subclavian artery • Brachial plexus Zone I Roon & Christensen Zones of the Neck • Clavicle to the cricoid cartilage: • Vertebral and carotid arteries • Major thoracic vessels • Apex of Lungs • Esophagus • Trachea • Spinal cord Zone II • Inferior margin of the cricoid cartilage to the angle of the mandible: • Vertebral and carotid arteries • Jugular veins • Esophagus • Trachea • Larynx • Spinal Cord Zone III • Angle of mandible to the base of the skull: • Vertebral and carotid arteries • Pharynx • Spinal cord Initial Management of Neck Trauma •ABC •Secure airway •Endotracheal intubation if needed •C-spine precautions •Cardiac monitoring •IV hydration •Surgical consultation •Close Neurological monitoring for changes Airway Management •Clinical Factors Indicating Need for Aggressive Airway Management • Acute respiratory distress • Airway Obstruction from blood/secretions • Massive subcutaneous emphysema of neck • Tracheal shift • Alteration in mental status • Expanding neck hematoma Initial Management of Neck Trauma Diagnostics to consider •First imaging study should be a portable chest XR to evaluate for pneumothorax, hemothorax, air in mediastinum •Non contrast CT of Cervical spine •Evaluate bony anatomy, fractures, vertebral body displacement •CTA (IV contrast) of neck •Evaluate vascular structures in the neck, ie. Dissections •Consider Hard and Soft signs S&S of Neck injury Hard Signs • Hypotension in ED • Active arterial bleeding • Diminished carotid pulse • Expanding hematoma • Thrill/bruit • Lateralizing signs • Hemothorax > 1000ml • Air or bubbling in wound • Hemoptysis • Hematemesis • Tracheal deviation Soft Signs • Hypotension in field • Hx of arterial bleeding • Unexplained bradycardia (without central nervous system injury) • Nonexpanding large hematoma • Apical capping on chest radiograph • Stridor • Hoarseness • Vocal cord paralysis • subQ emphysema • 7th CN injury Penetrating Neck Injuries •Stab wounds •Gun Shot wounds •Shrapnel •If the Platysma is violated, assume significant injury and immediate surgical consultation is indicated •Consider the zones in the neck and structures within those zones. •Never Probe neck wounds beneath the platysma •May disrupt hemostasis Algothrim for Penetrating Neck Injury Penetrating Neck Injuries Diagnosis and Management •Diagnostics: • If hemodynamically unstable, pulsatile bleeding and air or bubbling in wound pt needs emergent operation. If NOT proceed with further testing. • Non-contrast CT of Cervical spine to evaluate for fractures or foreign bodies • CTA (IV contrast) of neck to evaluate for vascular injures • Esophagram/endoscopy • Laryngoscopy/Bronchoscopy •Treatment: • Definitive treatment depends on findings and Zones of the neck Blunt Neck Injures • Motor vehicle collision…seatbelts • Pediatrics not properly seatbelted in! • “Clothesline” injury • Direct blow in a sports setting • Near hangings • Symptoms can be minimal or delayed • Edema • Laryngeal spasm • Hematoma • Can result in significant morbidity Strangulation Injures Manual Constriction Ligation Hanging • Cardiac arrest • Cervical spine fractures • Spinal cord injures • Cerebral anoxia • Carotid artery transection • Laryngeal fractures • Hyoid bone fractures • Venous congestion • Facial and conjunctival petechia Strangulation Injures Incomplete Hanging • Feet/body still in contact • Submandibular noose • Cerebral anoxia • Bradycardic cardiac arrest • Hanging can result in constriction of jugular venous obs leading to stagnant cerebral blood flow and brain ischemia and LOC • Arterial occlusion and or airway compromise results in death Complete Hanging • Feet off the ground • “Hangman’s Fracture” • Noose behind occiput • Patient drops the distance equal to their own height pt usually dies from FX of upper C-spine • Fracture of upper cervical spine • Spinal cord injury •Clinical Features of blunt or penetrating injuries: Layrngotracheal Injures • Dysphonia • Stridor • Hemoptysis • Hematemesis • Dysphagia • Neck emphysema • Dyspnea • Respiratory arrest Laryngotracheal Injury Carotid Injury • types on injury following: 1. 2. 3. Pseudoaneurysm Thrombosis Dissection • Clinical findings: • Hematoma, bruits, absent pulse, Horners syndrome, TIA, neuro deficits • Neuro deficits can be delayed for up to several weeks • Diagnostics: • Head and neck CTA Vascular Neck Injures • Etiologies of Carotid Artery Injuries 1. 2. 3. 4. 5. Hyperextension results in compression of carotid artery against the transverse process of the c-spine Hyperflexion results in compression of the artery between the mandible and the c-spine Direct blows Intraoral injuries Basilar skull fracture causing tearing of the intracranial portion of the carotid artery Dissection CT Head: Right Middle Cerebral Artery (MCA) infarction secondary to Right Carotid Dissection. Note loss of brain tissue (hypodense -dark area) CTA of Neck: No Contrast (white) is seen in Right Internal Carotid CTA of Neck: Short smooth tapering of Internal Carotid (no contrast extends past this point) Vertebral Artery Injury • Common mechanisms of injury: • chiropractic neck manipulation • Yoga exercises • Painting ceilings • Vertebral artery with its relationship with bony spine and ligaments cause its susceptibility to injury • Thrombotic occlusion, Hematoma, Dissection, or pseudoaneurysm formation Vertebral Artery Injuries • Clinical Features • • • • • • • Asymptomatic or transient symptoms Intermittent symptoms Delayed symptoms Headache Neck pain Ipsilateral facial paralysis Horner syndrome • Diagnostics • CTA of head and neck is the gold standard • Treatment: • anticoagulants to prevent stroke and thrombus • Surgery • stenting Vertebral Artery Esophageal Injures •Clinical Features • Dysphagia • Hematemesis •Diagnostics to r/o perforation • Fluoroscopic Esophagogram with Oral Contrast • CT scan Soft Tissue of Neck with IV contrast •Treatment • Surgical consultation • NPO • IV hydration Leakage of Oral contrast from esophageal perforation.