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Palliative > Dysphagia, Dyspepsia, Hiccup > Flashcards

Dysphagia, Dyspepsia, Hiccup Flashcards

1
Q

Definition of Dysphagia

A

Difficult swallowing, distinct from odynophagia (painful swallowing)

Oropharyngeal dysphagia - difficulty initiating swallow

Esophageal dysphagia - food bolus failing to easily traverse the esophagus

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2
Q

Physiology of normal swallowing

A
  1. Oral phase (voluntary control) - mastication
  2. Transfer phase - solid or fluid bolus pushed back into the pharynx by the tongue. As the bolus enters the hypopharynx, the involuntary swallow process begins
  3. Involuntary phase - bolus enters hypopharynx, larynx is elevated and pushed anteriorly to open the UES and allow the tongue to push the bolus into the esophagus.
  4. Esophageal phase - LES relaxes as the bolus enters the esophagus and a primary peristaltic contraction begins. Secondary peristaltic actions occur due to esophageal distention.
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3
Q

Oropharyngeal dysphagia - pathophys/causes

A

Occurs due to difficult transferring a bolus from the mouth to the pharynx, or from the pharynx to the esophagus

Causes:

  1. Structural
    - Malignancy
    - Enlarged thyroid
    - Zencker’s diverticulum
  2. Neurological
    - CVS, ALS, brain stem tumours, MS, Parkinsonism, neuropathy, dementia
  3. Myopathic
    - muscular dystrophy, polymysotisis, myasthenia, thyroid disease
  4. Iatrogenic
    - Meds causing myopathy (botox, amio, statins, vincristine)
    - Meds inhibiting saliva (opioids, TCAs, atropine, phenothiazine)
    - Rads to head and neck
    - Surgery to head and neck
  5. Poor dentition
  6. Anxiety
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4
Q

Effects of oropharyngeal dysphagia

A

Regurgitation, couching, choking.

High risk of aspiration, respiratory complications, malnourishment, dehydration.

Poor survival when compared to those without dysphagia

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5
Q

Aspiration - definition, outcome

A
  • Passage of food or fluids through the vocal cords leading to pneumonia
  • Severity of complications depends on type of aspirate and capacity to clear the pulmonary tree
  • Aspirations of solid can lead to fatal airway obstruction
  • Chemical pneumonia may occur if the aspirate is ascidic
  • Bacterial pneumonia may occur due to the normal flora of the mouth/pharynx
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6
Q

Esophageal dysphagia - definition/pathophys

A

Due to:

  • Narrowing of the lumen of the esophagus
  • Impaired motor function
  • Altered esophageal sensation

Causes:
1. Neuromuscular (achalasia, esophageal spasm, SLE, RA, IBD, scleroderma)

  1. Vascular (ischemic esophagus)
  2. Structural (stricture, diverticula, malignancy, external compression,
  3. Infectious: (mucosal injury secondary to infection - candidiasis, CMV, HIV)
  4. Meds: (causing mucusal injury - alendronate, NSAIDs, ascorbic acid, antibiotics)
  5. Eosinophilic esophagitis

Results in retention of the food or fluid bolus in the esophagus

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7
Q

Oropharyngeal dysphagia - prevalence

A
  • Common in older population, affecting up to 50% of adults in residential care
  • Not considered part of healthy ageing
  • High risk in CVA (25-50% with acute unilateral stroke, 60% likely to die due to consequences of dsyphagia)
  • Up to 80% in Alzheimers
  • 50-80% in PD
  • Esophageal CA
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8
Q

Epidemiology of esophageal cancer

A
  • May cause dysphagia

- At diagnosis, 50% have incurable disease

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9
Q

Presentation of oropharyngeal dysphagia

A
  • Difficulty initiating swallow
  • Swallowing repeatedly to effect pharyngeal clearance
  • Hoarse voice
  • Nasopharyngeal regurgitation
  • Coughing with swallowing
  • Sensation of food being ‘stuck’ (note can occur in esophageal dysphagia as well)
  • More trouble with thin fluids rather than swallowing
  • Weight loss, recurrent RTIs, pna, malnutrition with slower onset
  • With acute onset, more likely to be stroke
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10
Q

Presentation of esophageal dysphagia

A
  • Symptoms localised to chest
  • More likely to have difficulty with solids rather than thin liquids
  • May have chest pain with swallowing (especially if due to structural abnormality with reflux, narrowing of the lumen due to a structural abnormality, or a disorder of peristalsis).
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11
Q

Physical exam for dsphagia

A

Observation

  • Mental status (alertness, orientation)
  • Dysphonia or dysarthria (signs of motor dysfunction)

Oral cavity

  • Dentition (increased risk of asp pna)
  • Candidiasis

Neurologic exam (CN V, VII - XII)

  • Symmetry, strength, sensation of lips
  • Midline uvula
  • Gag reflex (stroke pharyngeal mucosa and ensure palatal retraction is symmetric - if abnormal, suggests bulbar pathology)
  • Tongue for wasting, fasciculations, deviation (deviates TOWARD lesion)
  • Cough

Observed swallowing test

  • How the patient opens their mouth, closes their mouth while taking fluid or solids
  • How well they are able to clear their mouth after swallowing
  • Whether the swallow changes with fatigue
  • Red flags (drooling, delayed swallow, coughing, wet or hoarse voice)

Respiratory exam

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12
Q

Investigation of oropharyngeal dysphagia

A
  • Nutrition parameters (albumin, CBC)
  • CT or MRI head if sudden onset
  • CXR (check for pna)

Barium video-fluoroscopy (swallow)

  • Localize the site of the swallowing difficulty
  • Visualizes all phase of swallowing and provides information to recommend the safest diet
  • Pt must be able to sit upright
  • Risk of aspiration

Flexible endoscopic evaluation of swallowing

  • Direct visualisation of the larynx and pharynx
  • Not as comprehensive as barium swallow, but no risk of aspiration
  • Oral phase of swallowing cannot be assessed
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13
Q

Investigation of esophageal dysphagia

A
  • Endoscopy for visualization of the esophagus, as well as biopsies, dilatation, and stent (Risk of perforation as a complication of biopsies or stent insertion)
  • Esophageal pH monitoring for reflux disease
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14
Q

Management of oropharyngeal dysphagia

A

Lifestyle changes

  • pureed diet (oral phase issues, food being pocketed in the buccal recesses, or pharyngeal retention of chewed solid food)
  • increasing number of chews and swallows per bolus
  • Thickened fluids
  • SLP for swallowing exercises (e.g. tongue to help with food bolus management, lips to help stop drooling, vocal cords to limit aspiration)
  • SLP for safe swallowing techniques (e.g. voluntary glottis closure, maneuvers)
  • Surgery in cases where life expectency is long and the case is pchronic
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15
Q

Principles of palliative management of dysphagia

A
  • Maximize swallowing function
  • Maintain adequate nutrition as appropriate to stage of life (particularly important when prognosis is long)
  • Allow people to participate in the social activities of eating/drinking
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16
Q

Prevention of aspiration pneumonia in dysphagia

A
  • Maintain nutrition and hydration (decreases risk of serious complications from aspiration pneumonia, particularly when immunocompromised or with impaired cough)
  • Ensuring good oral hygiene
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17
Q

When to consider enteral or parenteral feeds

A
  • When interventions are inadequate or inappropriate and a patient cannot maintain hydration or nutrition safely
  • Generally inserted for progressive debilitating conditions

Consider:

  • Reversibility of the swallowing problem
  • Degree to which underlying problem can be modified with less invasive interventions
  • Individual wishes of the patient
  • Risks
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18
Q

NG insertion - indications, risks, benefits

A
  • Least invasive (no sedation required), simplest
  • Recommended for situations where the need for enteral feeds are short or as a temporary measure

Risks:

  • bleeding, trauma, misplacement of the tube, esophageal perforation
  • Over time, discomfort, nasal ulceration, chronic sinusitis, reflux, aspiration pna
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19
Q

Oro-esophageal tube (indications)

A
  • Temporary placement of a narrow bore feeding tube only during a feed, then removed.
  • Useful for patients who do not have a gag reflex and decline other approaches to feeding
  • Requires compliance and time commitment
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20
Q

PEG tube - indications, risks

A

Percutaneous gastrostomy tube - tube inserted through the anterior abdominal wall

Surgical gastrostomy - requires general anesthetic

Percutaneous gastrostomy - sedation

Insertion complications:
- bleeding, infections, peritonitis, perforation of other organs

Risks:

  • Aspiration may still be a concern
  • Infections, tube leakage or displacement, bleeding, metabolic/biochemical consequences, microbial contamination of feeds
  • Survival at 12 months after starting enteral feeds is 40-50%

Contraindicated in patients with a short life expectancy

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21
Q

Treatment of esophageal strictures (dilatation)

A
  • Most commonly caused by reflux
Simple strictures (straight, less than 2cm, easily passed by scope)
- Dilatation alone
Complex strictures (longer than 2 cm, more tortuous, more difficult to pass the scope)
- Dilatation (commonly requires more than 3). If 7 attempts, may be stented

Risks of dilatation (rare - <1%)

  • Perforation
  • Bleeding
  • Bacteremia
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22
Q

Risk of stenting for esophageal strictures

A

Risks of stenting:

Mid-distal lesions

  • stent migration
  • Stent obstruction (food, benign or malignant overgrowth)
  • Reflux (+/- asp pna)

Proximal lesions (more challenging)

  • Food obstruction
  • Fistula formation
  • Aspiration

Up to 40% of patients experience complications within the first 2 months of stent insertion. Re-stenting typically successfull.

CANNOT stent a stricture that crosses the UES

23
Q

Palliation of malignant structures

A

Combination of dilatation, stent placement, adjuvant radiotherapy or brachytherapy depending on prognosis.

Dilatation
- May be done alone if prognosis is very short (e.g. < 3months)

Stenting

  • Typically offered for survival >3 months
  • Better immediate palliation, but longer term outcomes better with brachytherapy

Brachytherapy
- Single dose brachytherapy delivered by passing the appliance into the esophagus.

24
Q

Risks of brachytherapy for esophageal ca

A
  • Fistula formation
  • Stricture formation
  • Esophagitis
25
Q

Eosinophilic esophagitis (Dx, Tx)

A
  • Occurs as the result of inhaled allergens
    Treatment
  • Identification of allergen
  • Inhaled or systemic corticosteroids
26
Q

Treatment for esophageal spasm

A
  • Diltiazem
  • TCA antidepressants (imipramine)
  • Botox
  • Sildenafil (poor quality evidence)
27
Q

Management of oropharyngeal dysphagia when life is measured in months to years

A

Diet changes

  • Avoid thin liquids, very hard or very chewy foods
  • Pureed diet
  • Thickened fluids
  • Nutritional support
  • Ensure adequate fluid intake
  • Oral hygiene
  • Avoid meds contributing to dry mouth
  • Targeted exercises
  • Modification of swallowing behaviours (sitting upright, swallowing three times, fluids from a spoon, turning the head to one side to swallow if there is a weak side, ensuring residual food is removed from the oral cavity)
  • Surgery, enteral or parenteral feeds depending on severity
28
Q

Managing oropharyngeal dysphagia when life is measured in weeks

A
  • Diet
  • Positioning
  • Avoidance of meds likely to contribute to sedation
  • Oral care to improve dry mouth (may contribute to dysphagia)
  • Oral hygiene after meals to avoid aspiration
29
Q

Managing orpharyngeal dysphagia in the final stages of life

A
  • Oral hygiene

- DAT

30
Q

Managing orpharyngeal dysphagia in the final stages of life

A
  • Oral hygiene

- DAT

31
Q

Definition of dyspepsia

A

Epigastric pain, burning, postprandial fullness, or early satiety. Distinct from heartburn (retrosternal burning)

32
Q

Types of dyspepsia

A

Functional dyspepsia (no cause may be identified) versus secondary dyspepsia (e.g. GERD, PUD, gastric inflammatory conditions, UGI malignancy).

Functional dyspepsia is a diagnosis of exclusion.

33
Q

Stomach physiology

A
  • Function of stomach is to facilitate breakdown of solid food and empty into the small bowel along with indigestible solids.
  • Proximal stomach reflexively relaxes via vaga stimulation after swallowing, with increasing relaxation for increasing volumes
  • Concurrently, distal stomach contracts to allow the food to be broken down
  • Liquid is is emptied into the duodenum with coordinated contraction of the whole stomach, and is mediated by the pylorus
34
Q

Pathophysiology of dyspepsia

A

Disorder of gastric motility leading to changes in gastric emptying, though heterogeneous changes and poorly characterised.
- Larger gastric volumes lead to more marked distension and early satiety.

35
Q

Causes of dyspepsia

A

Functional

Secondary Dyspepsia

  • GERD
  • Esophagitis secondary to meds (opioids, iron, antibiotics, dig, CCBs, nitrates, bisphosphonates, NSAIDs, steroids)
  • PUD (h. pylori, NSAIDs)
  • Malignancy (esophageal or gastric ca)
  • Celiac disease
36
Q

Differential diagnosis for dyspepsia like symptoms

A

Infections (Giardia, strongyloides, TB)

Inflammatory
- Celiac, IBD, sarcoid

Infiltrative
- lymphoma, amyloid

Ischemic (chronic mesenteric or gastric ischemia)

Gastroparesis:

  • Idiopathic gastroparesis
  • Drug induced (opioids, anticholinergics)
  • Secondary gastroparesis (diabetes, hypothyroidism, autonomic neuropathy, systemic sclerosis)
37
Q

Presentation of dyspepsia

A
  • Post prandial fullness
  • Early satiety
  • Epigastric pain
  • Epigastric burning

May also include bloating, fullness, belching, N/V

Functional dyspepsia may be associated with IBS

38
Q

History for dyspepsia

A
  • Ask about IBS symptoms (constipation, diarrhea)
  • Consider if pain is improved by food (e.g. PUD)
  • Post prandial heartburn (reflux esophagitis)
  • Meds
  • Weight changes
  • Other changes to appetite
  • Vomiting of undigested food (flag for gastroparesis)
39
Q

Investigations of dyspepsia

A
  • Comprehensive history and physical

Excluding functional dyspepsia requires, at minimum, upper scope, 24 hr esophageal pH monitoring, H. pylori assessment

40
Q

Management of dyspepsia

A
  • Typically do not require medications, but will benefit from lifestyle modifications

Lifestyle

  • smaller, more frequent meals
  • Avoid food with high fat content
  • Avoid triggers

If severe sx, trial PPI. If ineffective after 8 weeks, consider a trial of a TCA (e.g. amitriptyline)

If bothered by postprandial fullness and early satiety, consider a prokinetic (metoclopramide, domperidone).

41
Q

Palliation of dyspepsia with prognosis of months to years

A
  1. Identify and treat any underlying causes
  2. Oral PPIs or H2 blockers for pain or burning
  3. Dietary changes (avoid high fat food, smaller, more frequent meals, avoid any triggers)
  4. Positioning
  5. Prokinetics if early satiety is a feature
  6. Supportive counselling, antidepressants if indicated
42
Q

Palliation of dyspepsia when life is measured in weeks

A
  1. Oral PPI or H2 blockers for pain or burning
  2. Dietary changes (avoid high fat food, smaller, more frequent meals, avoid any triggers)
  3. Positioning
  4. Prokinetics if early satiety is a feature
43
Q

Palliation of dyspepsia in final stages of life

A
  1. Parenteral PPI, H2 blockers

2. Parenteral metoclopramide

44
Q

Hiccups - definition

A
  • ‘Singultus’
  • Sharp and involuntary contraction of the muscles of inspiration, resulting in sharp inspiration and closure of the glottis
  • No identified physiologic purpose.
45
Q

Pathophysiology of hiccups

A
  • Afferent limb of phrenic (diaphragm) and vagus nerves and sympathetic chain
  • Central mediator (respiratory centre, medullar reticular formation, hypothalamus, phrenic nerve nuclei)
  • Efferent limb of the phrenic nerve - nerve connections to glottis (recurrent laryngeal nerve) and inspiratory muscles (phrenic nerve)

Sound made my a column of air evoked by the diaphragmatic contracting hitting the closed glottis

46
Q

Neurotransmitters involved in higgups

A
  • Likely numerous

- Most implicated are dopamine and GABA

47
Q

Causes of hiccups

A

Central

  • Vascular (stroke, aneurysm)
  • Space occupying lesions (tumour, abscess)
  • Head trauma
  • Encephalitis
  • Neurodegenerative (MS, PD)

Peripheral

  • Esophageal (dilatation, achalasia, tumour, food impaction)
  • GI (distention, gastritis, reflux, SBO, ascites, peritoneal traction)
  • Hepatic (liver mets/primary Ca, abscess, cholecystitis)
  • Iatrogenic (benzos, opioids, steroids, chemo)
  • Respiratory (diaphragmatic irritation - pna, effusion, subphrenic abscess)
  • Toxic/metabolic (renal failure, EtOH, lytes, hypoadrenalism)
  • Infectious (herpes zoster, GI candidiasis)
  • Cardiac (MI)
  • Psychological
48
Q

Presentation of hiccups

A
  • Frequency of 4-60 per minute, higher arterial CO2 tends to slow the frequency

If ~minutes, termed a ‘bout’

If >48 hrs, ‘protracted’

If >2 months “intractable”

Prolonged hiccups can cause significant distress, fatigue, anorexia, weight loss due to difficulty sleeping, eating and drinking, and causing vomiting. May also be associated with aspiration and pneumonia.

49
Q

Risk of hiccups in patients with a tracheostomy

A

May cause respiratory alkalosis secondary to hyperventilation (life threatening)

50
Q

Investigations of hiccups

A

Indicated for protracted courses of hiccups

  • Physical examination (neuro exam, abdo + liver exam, vitals, etc.)
  • Cr and urea (renal failure/uremia)
  • Lytes (hyponatremia, hypokalemia, hypocalcemia)
  • Liver based on PE
  • Imaging studies based on PE
51
Q

Medical palliation of hiccups

A

Warranted for hiccups >48 hrs
Consider Rx of underlying cause (e.g. PPI for GERD)

Empiric rx:

First line

  • Baclofen 5-10mg TID (smooth muscle relaxant)
  • Metoclopramide 10mg PO TID (dopamine antagonist)
  • Gabapentin 100mg TID (increasing GABA release)

Others
- Chlorpromazine 25mg PO TID (approved by FDA for intractable hiccups, but has more side effects and is no longer considered first line)

Typically, use for 5-10 days and stop the day after hiccups stopped. Some patients may require the medication indefinitely

52
Q

Non-pharm approaches to hiccups

A

For hiccups <48 hrs, based on case reports

  • Vagal nerve stimulation (case reports)
  • Acupuncture (low quality evidence)

Glottic stimulation
- Q tip or catheter stimulation of palate or pharynx

Vagal nerve stimulation

  • gargling/drinking ice water
  • Valsalva
  • living the uvula with a spoon
  • Traction on the tongue

Increase PaCO2

  • Breath holding
  • Breathing into a paper bag
53
Q

SLP following stroke

A
  • Dysphasia/Aphasia common post-stroke
  • Dysarthria very common
  • Dysphagia also common and predicted by aspiration within the first 72 hours
  • In the case of hemiparesis, client to turn head TOWARD weak side to divert food down to stronger side of the larynx

Palliative (71 decks)

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