Allergic Rhinitis

ALLERGIC RHINITIS

ESSENTIALS OF DIAGNOSIS

1. Characterized by sneezing, itching, rhinorrhea, and congestion.
2. May be seasonal, perennial, or both.
3. Can be associated with other chronic conditions, including asthma, otitis media with effusion (OME), rhinosinusitis, and nasal polyposis.
4. Typical symptoms of sneezing, rhinorrhea, and nasal congestion can be associated with viral, bacterial, allergic, and nonallergic etiologies
5. Can have multiple triggers, both inhaled and in­gested.

General Considerations
Allergy is a clinical manifestation of an adverse immune response after repeated contact with usually harmless substances such as pollens, mold spores, animal dander, dust mites, foods, and stinging insects. Allergic rhinitis is an inflammation of the nasal mucous membranes caused by an IgE-mediated reaction to one or more allergens. The prevalence of allergic rhinitis can vary considerably among age groups and locales.

Allergic rhinitis is one of the most common allergic diseases in the United States, affecting between 20% and 25% of the population (approximately 40 million people). Allergic rhinitis may have its onset at any age, but the incidence of onset is greatest in adolescence, with a decreasing incidence with advancing age. Its peak prevalence is during the third and fourth decades (Figure 1).

Figure 1. Prevalence of allergic rhinitis by age group.

The economic costs of allergic rhinitis, both direct and indirect, are considerable. The largest portion of the direct costs is the expenditure for both prescription and nonprescription medications (approximately 4 bil­lion dollars annually). The largest indirect costs are from both the allergy itself and also from the negative side effects of allergy medication (primarily over-the-counter antihistamines).

Although allergic rhinitis is not life threatening, its symptomatic effects are considerable, resulting in a sig­nificantly diminished quality of life for many sufferers. A number of quality of life studies have shown that in almost every facet of daily life, including social and physical functionality, energy and fatigue levels, and a lack of sleep and mental health, patients with allergic rhinitis have a significant loss of the quality of life com­pared with nonallergic individuals. In fact, patients with allergic rhinitis have been shown to have a lower quality of life than many asthmatics. In addition, aller­gic rhinitis may contribute to sleep disorders, fatigue, and—of particular importance with children—learn­ing problems.

Pathogenesis
The allergic response is mediated primarily by a type I hypersensitivity reaction. This response involves the excess production of IgE antibodies and is termed an atopic reaction. In addition to allergic rhinitis, most cases of asthma and atopic dermatitis are considered to have an atopic cause.

In patients with an atopic disposition (a genetic trait), an allergic reaction begins with sensitization to a specific allergen (in allergic rhinitis, these are usually airborne), which induces IgE-antibody production. This occurs through a T-cell, B-cell, and plasma cell cascade. On subsequent exposure, the specific antigen attaches to two specific IgE antibodies attached to the surface of mast cells, which are prevalent in the submu-cosa of the respiratory and gastrointestinal tracts, the subconjunctiva of the eye, and the subcutaneous layer of the skin. Consequently, this IgE-mediated reaction causes degranulation of the mast cell, which then pro­vokes an inflammatory response with the release of mediators such as histamine, leukotrienes, cytokines, prostaglandins, and platelet-activating factor. This is referred to as the early-phase or humeral reaction and occurs within 10–15 minutes of allergen exposure; the release of histamine causes the symptoms of sneezing, rhinorrhea, itching, vascular permeability, vasodilata-tion, and glandular secretion.

The release of cytokines and leukotrienes subsequently causes an influx of inflammatory cells (mainly eosinophils) into the affected area (chemotaxis). This inflammatory response is called the late-phase or cellular reaction, which can begin 4–6 hours after the initial sensitization and may prolong and enhance the allergic cascade for as long as 48 hours. This response is the main cause of the symptoms of nasal congestion and postnasal drip in allergic rhinitis.
In addition, these mediators produce a hyperreac-tion to both specific allergens and nonspecific irritants such as tobacco smoke and chemical fumes, referred to as the priming effect.

Causes
The development of atopy may be influenced by the following:

1. Genetic susceptibility (ie, family history);
   
2. Environmental factors (eg, dust and mold exposure);
3. Exposure to allergens (eg, pollens, animal dander, and foods);
4. Passive exposure to tobacco smoke (especially in early childhood); and
   
5. Diesel exhaust particles (in urban areas)—among other factors.

In infancy and childhood, food allergens such as milk, eggs, soy, wheat, dust mites, and inhalant allergies such as pet dander are the major causes of allergic rhinitis and the comorbidities of atopic dermatitis, otitis media with effu­sion, and asthma. In older children and adolescents, pol­len allergens become more of a causative factor.

Classification

A. Seasonal Allergic Rhinitis
The symptoms of seasonal allergic rhinitis, as its name implies, occur or are increased during certain seasons, usually depending on the pollination of plants to which the patient is allergic. Trees pollinate in the spring, grasses in the late spring and summer, and weeds in the fall. In addition, molds may cause symptoms in the fall. Characteristic symptoms of seasonal allergies include sneezing, watery rhinorrhea, itching of the nose, eyes, ears, and throat, red and watering eyes, and nasal congestion. Symptoms are usually worse in the morning and are aggravated by dry, windy conditions when higher concen­trations of pollen are distributed over a wider area.

B. Perennial Allergic Rhinitis
The symptoms of perennial allergic rhinitis are usually constant, with little seasonal variation, although they may vary in intensity. Characteristic symptoms are pre­dominantly nasal congestion and blockage, and postna-sal drip. Rhinorrhea and sneezing are less common. Eye symptoms are less common, except with animal aller­gies. Seasonal pollen may cause the exacerbation of any of these symptoms.

Common allergens that cause perennial allergic rhi­nitis are indoor inhalants, predominantly dust mites, animal dander, mold spores, and cockroaches (in inner cities). Certain occupational allergens may also cause perennial allergic rhinitis; these are not usually constant because they depend on workplace exposure.

Food allergens may also contribute to perennial allergic rhinitis. In addition, food allergies are often associated with other symptoms, including gastrointes­tinal problems, urticaria, angioedema, and even ana-phylaxis after food is ingested.

Infections and nonspecific irritants may influence perennial allergic rhinitis. In children with allergies, there may be a higher incidence of respiratory tract infections, which in turn tend to aggravate allergic rhinitis and may lead to the development of complications, especially rhi-nosinusitis and otitis media with effusion. Other irritants such as tobacco smoke, chemical fumes, and air pollutants can also aggravate symptoms.

C. Other Classifications
Recently, other classifications of allergic rhinitis have been introduced. One of these is related to both the temporal incidence and the quality of life. Symptoms are classified as being intermittent (<> 4 d/wk or > 4 weeks’ duration) and by the intensity of the symptoms, with either minimal or moderate to severe changes in the quality of life. In another classification system, symptoms are based accord­ing to the type of symptom (eg, patients who experience sneezing and a runny nose or those who are congested) without a temporal relationship.

Clinical Findings

A. Patient History
The diagnosis of allergic rhinitis should determine whether the patient is atopic and, if so, what the caus­ative allergen is. To determine these, a basic clinical evaluation should be performed, which should consist of a patient history, a physical examination, and confir­matory tests.

A careful history provides important clues for the diagnostician. Genetic factors determine the likelihood of an individual becoming sensitized and producing IgE antibodies (ie, being atopic). A family history of aller­gies, eczema, or asthma increases this possibility. Chil­dren with parents who have allergies have been shown to have a > 50% chance of becoming allergic themselves. If only one parent or a sibling has allergies, this rate is lower but still significant.

A thorough allergy history should determine whether symptom patterns are seasonal or perennial. Symptoms may include clear and watery nasal discharge, nasal con­gestion, postnasal drip, and itching of the nose, throat, and eyes. Persistent symptoms are presumed to be due to exposure to an indoor allergen. Seasonal symptoms or symptoms that are reproducible from an inciting factor, such as cat exposure, are most likely to be allergic. If the use of medication, especially antihistamines (both pre­scription and nonprescription) or intranasal corticoster-oids improves symptoms, allergy is probable. This is not the case with either intranasal or oral decongestants, which affect both allergic and nonallergic symptoms. A history of an anaphylactic reaction following ingestion of a particular food or being stung by an insect usually indi­cates an atopic patient.

Patients should be questioned about the onset, dura­tion, type, progression, and severity of their symptoms. A relationship to the seasons is important, with seasonal symptoms usually indicating a pollen allergy or possibly a mold allergy, but temperate climates can blur these seasonal distinctions. Perennial symptoms usually mean an allergy to dust mites, mold, or animals. An increase in symptoms at night usually suggests an allergy to dust mites or pet dander.
Associated ocular, pharyngeal, and systemic symp­toms, including recurrent rhinosinusitis, ear infections, asthma flare-ups, gastrointestinal symptoms, and skin rashes and hives, are important facts to ascertain in the history taking.
The patient should always be questioned about the impact of the symptoms on the quality of his or her life, because the correct diagnosis and, ultimately, sympto­matic relief from the appropriate treatment will play a large part in the functional impact on the patient’s life.

B. Physical Examination
A physical examination should include inspection of the ears, throat, and nasal passages (including after decongesting with a topical decongestant). Typical findings in the nose in patients with seasonal allergic rhinitis include bluish, pale, boggy turbinates; wet, swollen mucosa; and nasal congestion with nasal obstruction. With perennial allergies, nasal congestion is the predominant sign, but the nasal examination may appear normal. Anatomic abnormalities, such as a devi­ated nasal septum, concha bullosa, and nasal polyps, may be present. It should be determined whether these abnormalities are the main cause or merely contributing factors to the patient’s symptoms. If nasal polyps are suspected, an endoscopic nasal exam is also warranted. Other possible physical findings include conjunctivitis, eczema, and, possibly, asthmatic wheezing.

In children, allergic “shiners” (dark circles under the eyes), facial grimacing, mouth breathing, and the “nasal salute” (constant rubbing of the tip of the nose with the hand) are common physical findings. In addition, in this age group, a concomitant otitis media with effusion is also a possibility.

C. Special Tests

1. Allergy testing—Allergy testing is performed to establish objective evidence of atopic disease. It also can determine the causative allergens responsible, which would then lead to specific therapeutic recommenda­tions. Two major types of testing are available for iden­tifying and quantifying allergen sensitivity: skin testing and in vitro serum assays.
2. Skin testing—Skin testing can be epicutaneous, intradermal, or a combination of both.
   a. Skin prick test—The skin prick test is the most common epicutaneous test used. In general, it is a quick, specific, safe, and economical test. With new multitest systems available, it is an easy and simple office procedure to perform and also allows for unifor­ mity in the testing procedure. When a test result is equivocal, it is often followed by an intradermal test.
   b. Intradermal testing—Intradermal testing, using quantitative 1:5 serial dilutions, is the skin testingmethod of choice for most otolaryngic allergists. This type of testing, termed intradermal dilutional testing (IDT) and formerly known as serial endpoint titration (SET), is an excellent quantifier of allergen sensitivity, and, as such, is of significant benefit in the preparation of safe and cost-efficient immunotherapy treatment. Today, many otolaryngologists use the skin prick multitest as a screening test prior to performing IDT.
   
3. In vitro testing—Allergen-specific serum IgE test­ing is an easy and accurate method for determining the presence of atopic allergy, and with newer in vitro tech­nology available, in vitro testing is at least equivalent to skin testing in efficacy. In vitro assays are safe, specific, cost-effective, and reproducible, and do not require the patient to be free of antihistamines and other medica­tions that may interfere with skin testing. They are also easy and quick and are therefore preferred, especially in children and in anxious patients.
   Although the original in vitro assay, the RAST test (radioallergosorbent test), is no longer performed, its name is still used today to generally describe IgE-spe-cific blood testing. However, not all in vitro assays available today are alike. The newer assays tend to be faster, more reliable, and more efficient than previous tests. The ImmunoCap is an excellent example of this newer technology. Not using a reliable assay may affect the diagnosis of atopy and therefore the prescribing of appropriate therapy (Figure 2).
   In vitro testing can be cost-effective if an initial, appro­priately chosen inhalant screening battery of 10–12 aller­gens consisting of the most prevalent pollens, molds, dust mites, and animals in the local environment is used. In chil­dren, common allergenic foods are substituted or added. No further testing is necessary if this battery is negative. If the screening battery is positive and if no immunotherapy is considered, additional allergy testing can be performed.
   

Figure 2. In vitro testing process.

Differential Diagnosis
The differential diagnoses of allergic rhinitis include the fol­lowing:

1. Infectious rhinitis (acute or chronic);
2. Peren­nial nonallergic rhinitis (eg, vasomotor rhinitis);
3. Pollut­ants and irritants;
4. Hormonal rhinitis (eg, pregnancy or hypothyroidism);
   
5. Medication-induced topical rhinitis (rhinitis medicamentosa);
6. Anatomic deformity (eg, a deviated septum, nasal polyps, or a concha bullosa); and
7. Tumors or foreign bodies.

Treatment
The appropriate management of these common respira­tory diseases differs substantially, particularly when allergy is a contributing component. The treatment of allergic rhinitis must consider the main symptoms, their severity, the patient’s quality of life, the cost of therapy, as well as the allergens involved in order to individualize the patient’s treatment options. In addition, in the treatment of nasal allergies, consideration must be given to both the patient’s desire for rapid long-lasting relief of symptoms without side effects and the relief of any particular idio­syncratic symptoms, such as persistent rhinorrhea.

In general, three options are available for the manage­ment of allergic rhinitis:
(1) avoidance and environmental controls,
(2) pharmacotherapy, and
(3) immunotherapy.

A. Environmental Controls
Even if environmental controls are not complete, reduc­ing the allergic load may significantly decrease symp­toms. Methods of minimizing exposure to pollen are to avoid outdoor activities during relevant pollen seasons (eg, mowing the lawn and gardening), to keep home and car windows closed, and to use air conditioning when possible. To control dust mites, mold, and pet dander, the following practices should be used:
(1) reduce house­hold humidity to below 50%;
(2) wash bed linens in hot water;
(3) remove carpets and pets from the most often used living areas, especially bedrooms;
(4) encase pillows, mattresses, and box springs in hypoallergenic coverings (for dust mite protection); and
(5) in poor and urban set­tings, eliminate cockroaches (Table 1). For airborne allergens (eg, animal dander), air purifiers can be used.

B. Pharmacotherapeutic Measures
When selecting a pharmacologic treatment for allergic rhinitis, consideration must be given to the patient’s underlying condition, the likely pathophysiology, the dominant symptoms, the patient’s age and condition, the coexistence of related airway disorders, the patient’s preference, and the patient’s compliance history. In addition, before initiating any pharmacotherapy, the patient’s use and response to previous treatment should be considered (Table 2).

1. Antihistamines—Antihistamines are frequently used as a first-line therapy; many are available without a prescription. They block H1 receptor sites and pre­vent histamine-induced reactions, including inhibiting increased vascular permeability, smooth muscle con­traction, increased mucus production, and pruritus. Antihistamines also inhibit the “wheal and flare” response of the skin and therefore they affect skin testing unless withdrawn a few days before skin testing. They do not affect in vitro testing. Antihistamines are effective in early-phase reaction and therefore reduce sneezing, rhinorrhea, and itching. They have little effect on nasal congestion, a late-phase phenomenon.
   Nonprescription, first-generation antihistamines can cause sedation and impair performance and have been associated with a higher risk of both automobile and work-related accidents, decreased work performance and productivity, and impaired learning and academic performance. These side effects can be significantly exacerbated by alcohol, sedatives, antidepressants, and hypnotics. Many have anticholinergic effects and cause dry mouth. These include diphenhydramine (eg, Benadryl), hydroxyzine (eg, Atarax), chlorpheniramine, and brompheniramine. The latter two are found in most nonprescription cold remedies.
   Second-generation antihistamines have an antihista-mine activity comparable to that of first-generation antihistamines but have a better safety profile with lit­tle, if any, sedation as they have little affinity for central H1 receptors. They have no anticholinergic activity and are well absorbed, with a rapid onset of action and symptom relief usually within 1 hour. Second-genera­tion antihistamines are typically dosed once daily and are rarely associated with drug tolerance with prolonged use. Those available orally in the United States are fex-ofenadine (eg, Allegra), loratadine (eg, Claritin), deslor-atadine (eg, Clarinex), and cetirizine (eg, Zyrtec). A sec­ond-generation intranasal antihistamine, azelastine (eg, Astelin), is also available.
2. Intranasal corticosteroids—Intranasal corticoster-oids may be the most effective medications for the over­all control of allergic rhinitis symptoms. They relieve sneezing, itching, and rhinorrhea, and also nasal con­gestion. Maximal effect may take from 1 to 2 weeks after the onset of their use. Their effectiveness depends applica­tion. They act on the late-phase reaction and therefore prevent a significant influx of inflammatory cells. The newer formulations (mentioned below) have minimal systemic absorption with no systemic side effects, and they have been approved for use in children. They have no systemic side effects with regard to HPA axis sup­pression and do not affect long-bone growth in chil­dren. In young adults and children, they are considered the drugs of choice in the treatment of allergic rhinitis. Local side effects, such as dryness and epistaxis, can be reduced by careful patient instruction on their use and also the regular, concomitant use of intranasal saline. Commonly available intranasal corticosteroids in the United States include triamcinolone (eg, Nasacort), budesonide (eg, Rhinocort), fluticasone (eg, Flonase), and mometasone (eg, Nasonex).
   Table 1. Environmental control of indoor aeroallergens.
   

   Allergen	Environmental Control
   House dust mites	• Encase mattress, box spring, and pillows in occlusive covers • Wash all bedding in water > 130° F weekly • Dehumidify (<> • Remove reservoirs (especially carpeting)
   Pets	• Remove pet from home or at least from patient’s bedroom • Remove reservoirs (carpeting, stuffed furniture), if feasible • Wash animal frequent

3. Systemic corticosteroids—Systemic corticosteroids may be necessary for severe, intractable symptoms. They can be administered either by intramuscular injection or orally. With the latter, a tapering dose is usually given over 3–7 days. Systemic corticosteroids act on inflammation and significantly reduce all the symptoms of allergic rhinitis. The repeated use of these agents can cause serious side effects, such as HPA axis suppression, as well as other common side effects of steroid use.
   Table 2. Pharmacologic agents in the management of allergic rhinitis.
   

   Class	Mechanism of Action
   Antihistamines	Antagonize the H1 receptor–mediated effects of histamine
   Decongestants	Act predominantly on α-adrenergic recep­tors of the mucosa of the respiratory tract
   Intranasal and oral corticosteroids	Exert a wide range of effects on multiple cell types and mediators
   Mast cell stabilizers	Inhibit the release of mediators from mast cells
   Anticholinergic agents	Antagonize the action of acetylcholine at muscarinic receptors
   Leukotriene modifiers	Antagonize the action of leukotriene re­ceptors or inhibit 5-lipoxygenase and the formation of leukotrienes

   
   
4. Decongestants—Decongestants act on α-adrener-gic receptors of the nasal mucosa, producing vasocon-striction and thus reducing turbinate congestion. They improve nasal patency but do not relieve rhinorrhea, pruritus, and sneezing. These preparations are found mostly in nonprescription cold medicines and should be used with care in patients with cardiac problems and hypertension. Intranasal decongestants (eg, oxymetazoline) can cause rebound nasal congestion and cause dependency if used for more than 3–4 days (rhinitis medicamentosa).
5. Intranasal anticholinergics—These agents tend to control only rhinorrhea and have no other effects on allergy symptoms. One of the most commonly used intranasal anticholinergics is ipratropium bromide (eg, Atrovent). These agents can be combined with other allergic medications to control rhinorrhea in perennial allergic rhinitis.
6. Intranasal cromolyn—Intranasal cromolyn (eg, Nasalcrom) must be used before the onset of symptoms to be effective. This medication must be used through­out the entire exposure; it is considered to be very safe. The recommended dosage is four times daily.
7. Leukotriene inhibitors—Montelukast “Singulair” is a newer medication for the treatment of allergic rhi­nitis. To date, clinical studies have shown its efficacy to be greater than that of placebo, but less effective than antihistamines and intranasal steroids in the treatment of allergic rhinitis (Table 2).
   

C. Immunotherapy
Immunotherapy attempts to increase the threshold level of the appearance of symptoms after aeroallergen expo­sure. The exact mechanism of how immunotherapy works is still unclear; it may be the production of so-called “blocking” antibodies, as well as regulation of the immune cascade that causes allergic reactions.

Indications for immunotherapy include long-term pharmacotherapy for prolonged periods of time, the inadequacy or intolerability of drug therapy, and signif­icant allergen sensitivities. Before beginning immuno-therapy, the physician must first confirm the atopic diagnosis by testing IgE specific to the offending aller­gen (or allergens).

Most immunotherapy administered in the United States today is through a gradual increase in the dose of the antigen(s) given until either a mild systemic symptom or a large local reaction at the subcutaneous injection site occurs (optimal dose therapy). In some centers, sublingual immunotherapy is the method of choice. This is more common in Europe and tends to be easy and safe to administer at home by the patients themselves.

There is no adequate test available to indicate to the patient how long immunotherapy must be continued. Therefore, a clinical response with a reduction in symp­toms dictates the duration of specific treatment. A mini­mum of 2–3 years is usually given to avoid a rapid recur­rence of symptoms in uncomplicated allergic rhinitis.

D. Other Treatment Considerations
The first aspect of treating patients who have not responded well to therapeutic measures, including immunotherapy, is determining to what degree thera­peutic compliance has occurred. The next steps are to adjust drug dosages, try one or two other agents, and consider combination therapy. In addition, the physi­cian should determine whether allergy exposure has increased and should also review the environmental control measures. Finally, it may be necessary to recon­sider the diagnosis and reevaluate the patient.

Table 4. Pharmacotherapies for allergic rhinitis.

Agent	Inflammation	Congestion	Rhinorrhea	Sneezing	Nasal Itch	Ocular Symptoms
Antihistamines 1st generation 2nd generation	±	-	+ +	+ +	+ +	+ +
Topical antihistamines	±	±	+	+	+	±
Decongestants	-	+	-	-	-	-
Intranasal steroids	+	+	+	+	±	±
Oral steroids	+	+	+	+	±	+
Intranasal cromolyn	±	±	±	±	±	±

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Dizziness and Vertigo

Dizziness and Vertigo

Avery Hayes - Kochar's Clinical Medicine for Students, 5th Edition. 2008

Dizziness is one of the most common complaints in clinical practice and affects approximately 20% to 30% of the general population. This symptom is responsible for numerous visits to emergency departments and outpatient clinics. Ongoing dizziness can lead to a loss of function, falls, and injuries. Balance-related falls account for more than one half of all accidental deaths in the elderly. Dizziness is a nonspecific symptom and may be used by the patient to describe a number of different experiences. Because the differential diagnosis is broad, the evaluation of the dizzy patient can be both overwhelming and time consuming.

Differential Diagnosis

Dizziness may be classified into four broad categories based on clinical characteristics, which will provide for more accurate diagnosis (Table 1):

· Vertigo (Table 2) is the illusory sensation of spinning or motion. The patient may feel as if their body or the environment is in motion. Vertigo may be peripheral in etiology, due to disorders of the vestibular end organs (semicircular canals and utricle), eighth cranial nerve, or the vestibular nuclei. Central causes of vertigo include ischemia or damage to brainstem structures, or the cerebellum.

· Presyncope is the sense of impending loss of consciousness due to impaired cerebral blood flow, or anoxia, which often implies an underlying cardiovascular, metabolic, or hematologic disorder.

· Disequilibrium is a sense that one is about to fall, often associated with motor or sensory dysfunction resulting in the inability to maintain balance and gait.

· Lightheadedness describes other nonspecific symptoms related to multiple sensory disturbances, psychiatric illness, and medication side effects that alter the sensorium.

Vertigo

A crucial aspect of the evaluation of vertigo is to differentiate peripheral from central causes (Table 3. The latter have more serious consequences and require emergent evaluation and treatment. The clinical presentation, nature of the nystagmus, and presence of associated neurologic signs and symptoms may help distinguish vertigo of peripheral and central etiologies. Peripheral causes of vertigo often present as abrupt, intense attacks, which last several seconds to minutes, and are accompanied by nausea and vomiting. Vertigo due to central causes may occur with a more gradual onset but have a prolonged duration of symptoms. The intensity of symptoms may be less severe with central causes but often the patient may be unable to stand or walk. Nystagmus associated with peripheral vertigo can be decreased with visual fixation and is typically unidirectional (horizontal with a rotary component). Nystagmus that is purely vertical is due to a central cause. During cases of prolonged vertigo, nystagmus from peripheral causes is diminished by compensation and generally does not last longer than 48 hours.

Table 1 Differential diagnosis of dizziness

Dizziness subtype Type of sensation Temporal characteristics Differential diagnosis Vertigo Spinning or motion Episodic or continuous Benign paroxysmal positional vertigo Meniere’s disease Labyrinthitis Vertebrobasilar ischemia Cerebellar infarction or hemorrhage Presyncope Faint feeling, as though one were about to pass out Episodic, may last seconds, may be relieved by recumbent position Dehydration Ischemic heart disease Obstructive cardiac lesions Cardiac arrhythmia Neurocardiogenic syncope Anemia Hypoglycemia or hyperglycemia Infection Disequilibrium A sense of unsteadiness of the lower extremities Constant but may fluctuate in intensity Multiple sensory deficits including peripheral neuropathy and vision loss Lightheadedness Nonspecific Psychiatric conditions including anxiety, depression, panic attacks, and agoraphobia Hyperventilation Medications

Table 2 Differential diagnosis of vertigo

Peripheral vertigo Central vertigo Benign paroxysmal positional vertigo Cerebellar hemorrhage or infarct Acute vestibular neuritis Labyrinthitis Acoustic neuroma Meniere’sdisease Brainstem ischemia Vertebrobasilar insufficiency

Table 3 Characteristics of peripheral and central vertigo

Characteristics Peripheral Central Severity Severe Mild Onset Sudden Gradual Duration Seconds to minutes Weeks Positional Yes No Fatigable Yes No Associated symptoms Auditory Neurological and visual Nystagmus Horizontal Vertical From Chawala N, Olshaker JS. Diagnosis and management of dizziness and vertigo. Med Clin North Am 2006;90:291-304, with permission.

Because brainstem structures subserve many neurologic functions, infarcts causing vertigo will also have neighborhood effects due to injury to other cranial nerve nuclei, long motor, or sensory tracts. Common presentations are summarized in Table 4. Lateral medullary infarcts cause vertigo by infarction of the vestibular nuclei. Associated symptoms and signs include Horner's syndrome, ipsilateral facial numbness, diplopia, dysphagia, or contralateral limb numbness. Patients with cerebellar infarcts have signs such as dysmetria, past-pointing, or dysdiadochokinesis. Vertigo associated with transient ischemic attack due to vertebrobasilar artery (VBA) insufficiency is associated with additional symptoms such as diplopia, transient blindness, drop attacks, or dysarthria. Stroke in the VBA distribution may have a wide range of findings depending on the branch affected and collateral blood supply. Symptoms include hearing loss, ophthalmoplegia, blindness, sensory loss, and ataxia. Other processes affecting the cerebellum such as hemorrhage may present with headache, severe gait ataxia, or depressed levels of consciousness. The cerebellum may also be involved in demyelinating disorders such as multiple sclerosis.

Peripheral causes of vertigo are more common than central etiologies. Benign paroxysmal positional vertigo (BPPV) is the most common cause of peripheral vertigo. This condition occurs when debris form the utricle forms a plug and circulates within the endolymph of the semicircular canals. This clot is thought to act as a plunger and induce a push-and-pull force on the cupula, creating asymmetric impulses between both ears that result in vertigo and nystagmus. Most patients describe episodes of vertigo that are triggered by changes in head position, such as looking up or rolling over in bed. Attacks are usually sudden in onset and generally last less than 60 seconds. BPPV is characterized by fatigability. The patient will develop tolerance to repeated head movements, causing a reduction in continued symptoms.

Table 4 Stroke syndromes associated with vertigo

Site (artery) Clinical presentation Labyrinth (internal auditory artery) Lateral medullary infarct (vertebral artery, posterior inferior cerebellar artery) Lateral pontomedullary infarction (anterior inferior cerebellar artery) Cerebellum (posterior and anterior inferior cerebellar arteries, superior cerebellar artery) Tinnitus, hearing loss Horner's syndrome, cranial nerves V and VII, crossed sensory loss Horner's syndrome, cranial nerves V and VII, crossed sensory loss, hearing loss Limb dysmetria, ataxia From Delaney K. Bedside diagnosis of vertigo: value of the history and neurologic examination. Acad Emerg Med 2003;10:1388-1395, with permission.

Labyrinthitis and vestibular neuritis are characterized by inflammation; either the canals of the inner ear, vestibular nerve, or nuclei can be affected. Both syndromes can follow a viral upper respiratory infection. Patients usually present with severe vertigo, nausea, and vomiting. Symptoms usually last from days to weeks. The vertigo gradually subsides as the inflammation resolves and central compensatory mechanisms evolve. Otitis media may cause a suppurative labyrinthitis due to bacterial spread form the middle ear through a ruptured membrane or perilymph fistula. These patients appear acutely ill and present with hearing loss and fever in addition to nausea, vomiting, and vertigo. Ramsay-Hunt syndrome is caused by Varicella zoster and is a variant of vestibular neuritis with involvement of the cranial nerves VII and VIII, causing facial paresis, tinnitus, hearing loss, and vertigo.

Meniere’s disease is due to an increase in the volume of endolymph, causing distention of the endolymphatic system. The classic triad is vertigo, tinnitus, and fluctuating sensorineuronal hearing loss. Attacks of vertigo are abrupt and may last from minutes to hours. Attacks also vary in intensity and may be associated with aural fullness or pain. Symptoms can be unilateral or bilateral.

Acoustic neuroma is a benign tumor composed of Schwann cells of the vestibular nerve. Patients often present with tinnitus and hearing loss. These tumors are slow growing and central compensation leads to less severe vertigo. Enlargement of the tumor within the cerebellopontine angle causes compression of the adjacent cranial nerves and brainstem, and may result in facial anesthesia and weakness.

Presyncope

As noted above, presyncope is the sensation that one is about to lose consciousness. Often, this is a milder manifestation of an event that ultimately could result in true syncope. The differential diagnosis and evaluation are the same as for syncope.

Disequilibrium

Dysequilibrium syndrome should be suspected when a patient feels unsteady, as though they are about to fall. This sensation is particularly prominent following a sudden change in position or with loss of visual cues, as when getting on or off an elevator. This phenomenon is triggered by loss of sensory inputs that cue the brain to position or the loss of musculoskeletal function interfering with the minor readjustments in position to maintain balance.

Disequilibrium can be seen in association with a number of disorders including peripheral neuropathy, visual impairment, severe arthritis, and Parkinson's disease. It is particularly common in patients with long-standing diabetes who may have several of these issues present simultaneously.

Lightheadedness

A substantial number of patients with dizziness describe relatively vague symptoms that are difficult to verbalize. Oftentimes these are characterized as a sensation of being lightheaded or floating. A majority of these patients have an underlying psychological issue including anxiety, depression, or increased stress. Physical examination is usually unremarkable. In some of these patients, subclinical hyperventilation may play a role.

Evaluation

Some patients may not be able to give an accurate history; therefore, the physical examination not only serves to differentiate peripheral from central causes of vertigo, but also helps to evaluate for causes of dizziness other than vertigo. Vital signs should be measured, including orthostatic blood pressure.

Physical examination should include a complete eye, ear, nose, and throat examination (looking for nystagmus, asymmetry, or defects in the pupillary reactivity and extraocular movements) and a funduscopic examination to check for papilledema. Inspection of the tympanic membranes should be performed to evaluate for scarring, fluid, or infection. If hearing loss is detected, the Weber and Rinne tuning fork examinations can differentiate between conductive and sensorineural hearing loss. Auscultation for carotid bruits and cardiac examination should be performed to evaluate for potential sources of emboli or obstructive cardiac lesions. A thorough neurological examination is important, including examination of motor strength and sensation, cranial nerves, cerebellar function, Rhomberg's test, and gait.

The Dix-Hallpike maneuver is used to diagnose BPPV (Fig. 1). The patient is seated upright on the examining table with the head held in the hands of the examiner for support. The patient's head is turned 45 degrees toward the side being tested. The patient is rapidly lowered to a supine position with the head hanging below the level of the examining table. The patient should be reminded to keep the eyes open because it is critical to see if vertigo occurs. After a short period of latency, a positive test is indicated by a burst of torsional-vertical nystagmus (the upper poles of the eyes beat torsionally toward the ground) associated with vertigo. The vertigo typically lasts between 20 to 40 seconds and is pathognomonic of the posterior canal variant of BPPV.

Figure 1 Dix-Hallpike maneuver. The patient is positioned with the head hanging 30 to 45 degrees over the table edge first in the midline, which is repeated with the head rotation to right and left. Frames one through four show the procedure in sequence.

If disequilibrium is suspected, it can be helpful to perform a finger touch test. The physician attempts to reproduce the symptom by having the patient turn or change position quickly. In the presence of the symptom, the patient is asked to touch the examiner's finger with their own. If the symptoms improve dramatically, it is very suggestive of disequilibrium.

If the complaint is lightheadedness, the patient should be asked to deliberately hyperventilate. If the symptoms are reproduced, this can help confirm the diagnosis and be used as a tool to reassure the patient.

Laboratory tests may not be helpful if the dizziness is caused by vertigo, but may indicate another cause. Complete blood counts, basic metabolic panel, and thyroid function tests may indicate the presence of anemia, electrolyte abnormalities, hypoglycemia, dehydration, or thyrotoxicosis causing symptoms. Electrocardiography may show signs of atrial fibrillation or ischemia.

Electronystagmography is an examination that records eye movements in response to vestibular, visual, cervical, caloric, rotational, and positional stimulation, and may be used to assess vestibular function. Audiologic evaluation can be performed if indicated to evaluate for patterns of hearing loss.

Patients with suspected central cause of vertigo require cranial imaging with either computed tomography (CT) or magnetic resonance imaging (MRI). CT will identify cerebellar hemorrhage or infarction and suggest the presence of tumor, but lacks the sensitivity to detect small infarcts in the brainstem. MRI has superior sensitivity and will identify small lesions including infarcts, tumors, and plaques. Magnetic resonance angiography will visualize the intracranial vasculature, including the vertebrobasilar system. Patients suspected of having an infarct should also be evaluated for a source of thromboembolism, including electrocardiogram to rule out atrial fibrillation and echocardiogram with a bubble study to evaluate for intracardiac shunt.

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Gaster Anatomy II

VASCULAR SUPPLY AND LYMPHATIC DRAINAGE

ARTERIES

The arterial supply to the stomach comes predominantly from the coeliac axis although intramural anastomoses exist with vessels of other origins at the two ends of the stomach (Figs 8, 9). The left gastric artery arises directly from the coeliac axis. The splenic artery gives origin to the short gastric arteries as well as the left gastroepiploic artery and may occasionally give origin to a posterior gastric artery. The hepatic artery gives origin to the right gastric artery and the gastroduodenal artery, which in turn gives origin to the right gastroepiploic artery.

Left gastric artery

The left gastric artery is the smallest branch of the coeliac axis. It ascends to the left of the midline and crosses the left crus of the diaphragm beneath the peritoneum of the upper posterior wall of the lesser sac. Here it lies adjacent to the left inferior phrenic artery and medial or anterior to the left suprarenal gland. It runs forwards into the superior portion of the lesser omentum adjacent to the superior end of the lesser curvature. It turns anteroinferiorly to run along the lesser curvature between the two peritoneal leaves of the lesser omentum. At the highest point of its course, it gives off an oesophageal branch. In its course along the lesser curvature, it gives off multiple branches that run onto the anterior and posterior surfaces of the stomach and anastomose with the right gastric artery in the region of the incisura angularis.

The left gastric artery may arise from the common hepatic artery or its branches. The most common variant is an origin from the left hepatic artery, when the left gastric artery passes between the peritoneal layers of the superior lesser omentum to reach the lesser curvature of the stomach. Other variants include a common origin with the common hepatic artery. An aberrant left hepatic artery can occasionally arise from the left gastric artery: identification of an aberrant origin may be of importance during surgical mobilization of the upper stomach.

Short gastric arteries

The short gastric arteries are variable in number, commonly between five and seven, and arise from the splenic artery, its divisions, or from the proximal left gastroepiploic artery. They pass between layers of the gastrosplenic ligament to supply the cardiac orifice and gastric fundus, and anastomose with branches of the left gastric and left gastroepiploic arteries. An accessory left gastric artery may arise with these vessels from the distal splenic artery.

Left gastroepiploic artery

The left gastroepiploic artery arises from the splenic artery as its largest branch near the splenic hilum. It runs anteroinferiorly between the layers of the gastrosplenic ligament and into the upper gastrocolic omentum. It lies between the layers of peritoneum close to the greater curvature, running inferiorly to anastomose with the right gastro epiploic artery. It gives off gastric branches to the fundus of the stomach through the gastrosplenic ligament and to the body of the stomach through the gastrocolic omentum. These are necessarily longer than the gastric branches of the right gastroepiploic artery and may be 8-10 cm long. Epiploic (omental) branches arise along the course of the vessel and descend between the layers of the gastrocolic omentum into the greater omentum. A particularly large epiploic branch commonly originates close to the origin of the left gastroepiploic artery, descends in the lateral portion of the greater omentum and provides a large arterial supply to the lateral half of the omentum.

Posterior gastric artery

Variant:
A distinct posterior gastric artery may occur. When present, it arises from the splenic artery in its middle section posterior to the body of the stomach. It ascends behind the peritoneum of the lesser sac towards the fundus. It reaches the posterior surface of the stomach in the gastrophrenic fold.

Right gastric artery

The right gastric artery arises from the hepatic artery as it passes forwards from the posterior wall of the lesser sac into the lower border of the lesser omentum above the first part of the duodenum. The right gastric artery then runs between the peritoneal layers of the lesser omentum just above the medial end of the lesser curvature. It passes superiorly along the lesser curvature, giving off multiple branches onto the anterior and posterior surfaces of the stomach, and anastomoses with the left gastric artery.

The origin of the right gastric artery is often variant. The most common alternative origins are from the common hepatic, left hepatic, gastroduodenal or supraduodenal arteries.

Figure 8 Arterial supply of the stomach

Gastroduodenal artery

The gastroduodenal artery arises from the common hepatic artery posterior and superior to the first part of the duodenum. It gives origin to the right gastroepiploic and superior pancreaticoduodenal arteries at the lower border of the first part of the duodenum.
Right gastroepiploic artery

The right gastroepiploic artery originates from the gastroduodenal artery behind the first part of the duodenum, anterior to the head of the pancreas. It passes inferiorly towards the midline between the layers of the gastrocolic omentum. It lies inferior to the pylorus and then runs laterally along the greater curvature. It ends by anastomosing with the left gastroepiploic artery. It is adjacent to the pylorus but, more distally, lies c.2 cm from the greater curvature of the stomach. Gastric branches ascend onto the anterior and posterior surfaces of the antrum and lower body of the stomach while epiploic branches descend into the greater omentum. It also contributes to the supply of the inferior aspect of the first part of the duodenum.

Arterial anastomoses of the stomach

There is an anastomosis between the oesophageal arteries originating from the thoracic aorta and the vessels supplying the fundus in the region of the cardiac orifice. At the pyloric orifice the extensive network of vessels supplying the duodenum allows for some anastomosis between vessels of superior mesenteric artery origin and the pyloric vessels. The major named vessels supplying the stomach form extensive arterial anastomoses both on the serosal surface and around the curvatures. The right and left gastroepiploic arteries and the left and right gastric arteries anastomose freely with each other along the greater and lesser curvatures respectively. Anastomoses also form between the short gastric and left gastric arteries in the region of the fundus, and between the right gastric and right gastroepiploic arteries in the region of the antrum. In addition to the extensive serosal anastomoses, networks form within the stomach wall at intramuscular, submucosal and mucosal levels. A true plexus of small arteries and arterioles is present within the submucosa: it supplies the mucosa and shows considerable regional variation both in the gastric wall and in the proximal duodenum. The rich arterial supply to the stomach ensures that the high mucosal blood flow required for physiological functioning is maintained even if one or more vessels become occluded. As a consequence, the stomach exhibits considerable resistance to ischaemia even when multiple arterial supplies are lost.

The pyloric arteries are rami of the right gastric and right gastroepiploic arteries and pierce the duodenum distal to the sphincter around its entire circumference. They pass through the muscular layer to the submucosa where they divide into two or three rami, which turn back into the pyloric canal beneath the mucosa and run to the end of the pyloric antrum . They supply the entire mucosa of the pyloric canal. Branches of these pyloric submucosal arteries may anastomose close to their origin with the duodenal submucosal arteries. Their terminal rami also anastomose with gastric arteries from the prepyloric antrum. The pyloric sphincter is supplied by the gastric and pyloric arteries via rami that leave their parent vessels in the subserosal and submucosal levels to penetrate the sphincter.

Dieu la Foy lesions

Abnormalities of the intramural vascularity of the stomach are a rare cause of bleeding from the upper gastrointestinal tract. So-called 'Dieu la Foy' lesions commonly occur in the proximal body or fundus. When not actively bleeding, they appear as small, raised, red dots marking the mucosal surface of the proximal body or fundus. They were originally thought to be small arteriovenous malformations of the submucosal plexus. It is now considered that such lesions are caused by a larger than normal penetrating arterial vessel running through the muscular coat of the stomach into the submucosa before branching into the submucosal plexus. Although not a pathological abnormality, the vessel has a greater than normal calibre for arteries at this level. The pulsatile flow, combined with its proximity to the overlying mucosa, may then lead to focal ulceration and rupture of the vessel following minor trauma, leading to profuse intraluminal bleeding.

VEINS

The stomach veins drain ultimately into the portal vein. A rich submucosal and intramural network of veins gives rise to veins that usually accompany the corresponding named arteries. They drain either into the splenic or superior mesenteric veins although some pass directly into the portal vein.

Short gastric veins

Four or five short gastric veins drain the gastric fundus and the upper part of the greater curvature. They drain into the splenic vein or one of its large tributaries.

Left gastroepiploic vein
The left gastroepiploic vein drains both anterior and posterior gastric surfaces and the adjacent greater omentum. It runs superolaterally along the greater curvature, between the layers of the gastrocolic omentum. It receives multiple tributaries from the anterior and posterior surfaces of the body of the stomach and the greater omentum, and drains into the splenic vein within the gastrosplenic ligament.

Right gastroepiploic vein
The right gastroepiploic vein drains the greater omentum, distal body and antrum of the stomach. It passes medially, inferior to the greater curvature, in the upper portion of the gastrocolic omentum. Just proximal to the pyloric constriction it passes posteriorly to drain into the superior mesenteric vein below the neck of the pancreas. It may receive the superior pancreaticoduodenal vein close to its entry into the superior mesenteric vein.

Left gastric vein
The left gastric vein drains the upper body and fundus of the stomach. It ascends along the lesser curvature to the oesophageal opening where it receives several lower oesophageal veins. It then curves posteriorly and medially behind the posterior peritoneal surface of the lesser sac. It drains into the portal vein directly at the level of the upper border of the first part of the duodenum.

Right gastric vein
The right gastric vein is typically small and runs along the medial end of the lesser curvature. It passes under the peritoneum as it is reflected from the posterior aspect of the pylorus and first part of the duodenum onto the posterior wall of the lesser sac. It drains directly into the portal vein at the level of the first part of the duodenum. It receives the prepyloric vein as it ascends anterior to the pylorus at the level of the pyloric opening.

Posterior gastric veins
Distinct posterior gastric veins may occur. When present, they accompany the posterior gastric artery from the middle of the posterior surface of the stomach. They drain into the splenic vein and may occur as multiple small vessels.

Gastric varices
Variceal dilatation of the submucosal veins of the stomach may occur in the presence of portal hypertension. The anastomosis between portal and systemic venous circulations occurs around the lower oesophagus and upper stomach. Submucosal veins close to the cardiac orifice may become involved in the pathological flow of blood from the stomach and other upper abdominal viscera into the oesophageal veins. Gastric varices present less commonly in clinical practice than oesophageal varices. Occasionally gastric varices exist without the presence of oesophageal varices. In these circumstances, it may be that the effective 'point of meeting' between portal and systemic venous systems is lower than usual and occurs in the upper stomach rather than the lower oesophagus.

LYMPHATIC DRAINAGE

The stomach has a rich network of lymphatics that connect with lymphatics draining the other visceral organs of the upper abdomen. At the gastro-oesophageal junction the lymphatics are continuous with those draining the lower oesophagus. In the region of the pylorus they are continuous with those draining the duodenum. In the main, they follow the course of the arteries supplying the stomach, however many separate node groups are now recognized (Fig. 11). The relationship of separate node groups to the regions of the stomach and the vascular territories supplied is of great importance during resection of the stomach, particularly for malignancy. Pancreatic and hepatic lymphatics play a considerable role in draining areas of the stomach during disease.

Figure 9 Lymph node stations of A, the stomach and B, upper abdominal viscera.

INNERVATION

The stomach is innervated by sympathetic and parasympathetic fibres. The sympathetic supply originates from the fifth to twelfth thoracic spinal segments and is mainly distributed to the stomach via the greater and lesser splanchnic nerves and the coeliac plexus. Periarterial plexuses form along the arteries and supply the stomach from the coeliac axis. Additional innervation comes from fibres of the hepatic plexus, which pass to the upper body and fundus via the upper limit of the lesser omentum. Some innervation is also provided via direct branches from the greater splanchnic nerves.

The parasympathetic supply is from the vagus nerves (Fig. 10). Usually one or two rami branch on the anterior and posterior aspects of the gastro-oesophageal junction. The anterior nerves are mostly from the left vagus and the posterior from the right vagus, both emerging from the oesophageal plexus.

The anterior nerves supply filaments to the cardiac orifice and divide near the oesophageal end of the lesser curvature into gastric, pyloric and hepatic branches. Gastric branches (between four and ten) radiate on the anterior surface of the body and fundus. The greater anterior gastric nerve is the major gastric branch and lies in the lesser omentum near the lesser curvature. Pyloric branches (generally two) originate below the cardiac orifice. The smaller of the two nerves runs between the peritoneal layers of the lesser omentum almost horizontally towards its free edge and turns down on the left side of the hepatic artery to reach the pylorus. The larger nerve usually arises from the greater anterior gastric nerve during its course over the anterior surface of the stomach and runs inferomedially to the pyloric antrum. Hepatic branches (one or two) originate from the pyloric branches and run superiorly to contribute to the hepatic plexus.

The posterior nerves produce two main groups of branches, gastric and coeliac. Gastric branches originate behind the cardiac orifice and upper body of the stomach. They radiate over the posterior surface of the body and fundus and extend to the antrum but do not reach the pyloric sphincter. The largest is termed the greater posterior gastric nerve and runs posteriorly along the lesser curvature, giving branches to the coeliac plexus. Coeliac branches are often larger than the gastric branches. They run beneath the peritoneum, deep to the posterior wall of the lesser sac, at the upper limit of the lesser omentum to reach the coeliac plexus. Hepatic branches (one or two) are often small and originate from the coeliac branches. No true plexus occurs on either the anterior or posterior gastric surfaces, but plexuses are present in the submucosa and between the layers of the muscularis externa.

The gastric sympathetic nerves are vasoconstrictor to the gastric vasculature and inhibitory to gastric musculature. The sympathetic supply to the pylorus is motor, and brings about pyloric constriction. The sympathetic supply also conducts afferent impulses that mediate sensations, including pain. The parasympathetic gastric supply is secretomotor to the gastric mucosa and motor to the gastric musculature. It is also responsible for coordinated relaxation of the pyloric sphincter during gastric emptying.

Coeliac plexus

The coeliac plexus is the largest major autonomic plexus, sited at the level of the twelfth thoracic and first lumbar vertebrae. It is a dense network uniting two large coeliac ganglia and surrounds the coeliac artery and the root of the superior mesenteric artery (Fig. 13). It is posterior to the stomach and lesser sac, anterior to the crura of the diaphragm and the commencement of the abdominal aorta, and lies between the suprarenal glands. The plexus and ganglia are joined by greater and lesser splanchnic nerves and branches from the vagus and phrenic nerves. The plexus extends as numerous secondary plexuses along adjacent arteries.

The coeliac ganglia are irregular masses on each side of the coeliac trunk adjacent to the suprarenal glands. They lie anterior to the crura of the diaphragm. The right ganglion is posterior to the inferior vena cava, the left ganglion posterior to the origin of the splenic artery. The ipsilateral greater splanchnic nerve joins the upper part of each ganglion. The lower part of each ganglion forms a distinct subdivision usually termed the aorticorenal ganglion. This receives the ipsilateral lesser splanchnic nerve and gives origin to the majority of the renal plexus. It most commonly lies anterior to the origin of the renal artery. The coeliac plexus is connected to or gives rise to the phrenic, splenic, hepatic, superior mesenteric, suprarenal, renal and gonadal plexuses.

Phrenic plexus

The phrenic plexus lies around the inferior phrenic arteries on the crura of the diaphragm. It arises as a superior extension of the coeliac ganglion and often receives one or two sensory branches from the phrenic nerve. The left phrenic plexus is usually larger than the right. On the left it supplies branches to the left suprarenal gland and the cardiac orifice of the stomach. The right phrenic plexus joins the phrenic nerve, forming a small phrenic ganglion. This distributes branches to the inferior vena cava, suprarenal gland and hepatic plexus.

Figure 10 Distribution of the vagal nerves to the stomach.

REFERRED PAIN
The majority of the sensation of pain arising from the stomach is poorly localized. In common with other structures of foregut origin, it is referred to the central epigastrium. Pain arising from the region of the gastro-oesophageal junction may involve innervation from the oesophagus and is commonly referred to the lower retrosternal and subxiphoid areas.

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Gaster Anatomy I

STOMACH ANATOMY I

Gray's Anatomy 39th

The stomach is the widest part of the alimentary tract and lies between the oesophagus and the duodenum. It is situated in the upper abdomen, extending from the left upper quadrant downwards, forwards and to the right, lying in the left hypochondriac, epigastric and umbilical areas. It occupies a recess beneath the diaphragm and anterior abdominal wall that is bounded by the upper abdominal viscera on either side. Its mean capacity increases from c.30 ml at birth, to 1000 ml at puberty, to c.1500 ml in adults. The peritoneal surface of the stomach is interrupted by the attachments of the greater and lesser omenta, which define the greater and lesser curvatures separating two surfaces

PARTS OF THE STOMACH

The stomach is divided for descriptive purposes into the fundus, body, pyloric antrum and pylorus, by arbitrary lines drawn on its external surface. The internal appearance and microstructure of these regions varies to some degree. The fundus is dome shaped and projects above and to the left of the cardiac orifice to lie in contact with the left dome of the diaphragm. It lies above a line drawn horizontally from the incisura cardiaca to the greater curvature. The body extends from the fundus to the incisura angularis, which is a constant external notch at the lower end of the lesser curvature. A line drawn from the incisura angularis to an indentation on the greater curvature defines the lower boundary of the body. The pyloric antrum extends from this line to the sulcus intermedius. At this point, the stomach narrows to become the pyloric canal, which is usually only 1-2 cm in length and terminates at the pyloric orifice.

Figure 1 The parts of the stomach.

GASTRIC RELATIONS

GASTRIC CURVATURES

Lesser curvature

The lesser curvature extends between the cardiac and pyloric orifices and forms the medial (posterior and superior) border of the stomach. It descends from the medial side of the oesophagus in front of the decussating fibres of the right crus of the diaphragm. It curves downwards and to the right and lies anterior to the superior border of the pancreas. It ends at the pylorus just to the right of the midline. In the most dependent part there is typically a notch, the incisura angularis, whose position and appearance vary with gastric distension. The lesser omentum is attached to the lesser curvature and contains the right and left gastric vessels.

Greater curvature

The greater curvature is four or five times longer than the lesser. It starts from the incisura cardiaca formed between the lateral border of the abdominal oesophagus and the fundus of the stomach. It arches upwards, posterolaterally and to the left. Its highest convexity, the apex of the fundus, is approximately level with the left fifth intercostal space just below the left nipple in males, but varies with respiration. From this level it sweeps inferiorly and anteriorly, slightly convex to the left, almost as far as the tenth costal cartilage in the supine position, where it turns medially to end at the pylorus. There is frequently a groove, termed the sulcus intermedius, in the curvature close to the pyloric constriction. The start of the greater curvature is covered by peritoneum, which continues over the anterior surface of the stomach. Laterally the greater curvature gives attachment to the gastrosplenic ligament and beyond this to the greater omentum, which contains the gastroepiploic vessels. The gastrosplenic ligament and the greater omentum, together with the gastrophrenic and splenorenal ligaments, are continuous parts of the original dorsal mesogastrium. The names merely indicate regions of the same continuous sheet of peritoneum and associated connective tissue.

Gastric volvulus

Volvulus of the stomach is much less common than volvulus of either the sigmoid colon or caecum. Two types of gastric volvulus may occur. The first, organoaxial volvulus, occurs about a line of rotation running from below the cardiac orifice to the pylorus. The antrum, body and fundus rotate upwards, with the greater curvature coming to lie above the lesser curvature as the volvulus progresses. The second, mesenteroaxial volvulus, occurs about a line drawn 'across' the body of the stomach, usually just above the incisura angularis. This type of volvulus is perpendicular to the line of organoaxial volvulus. The distal body and antrum rotate anteriorly, superiorly and laterally whilst the upper body and fundus rotate posteriorly, medially and inferiorly. Although relatively mobile within the upper abdomen, the stomach is normally tethered to the oesophagus at the gastro-oesophageal junction, to the duodenum at the pylorus, to the spleen by the gastrosplenic omentum, and to the liver by the lesser omentum. The attachment to the transverse colon via the gastrocolic omentum also restrains the stomach but is the most mobile of all. For either type of gastric volvulus to occur, it is necessary for some or all of these points of tethering to be loosened either by previous surgical division or by chronic lengthening and loosening of their connective tissue. Organoaxial volvulus is most common because the lesser omentum, gastrosplenic ligament and gastrocolic omentum are more likely to undergo chronic lengthening by traction than the other attachments of the stomach. Mesenteroaxial volvulus requires the gastro-oesophageal junction and pylorus to be sufficiently mobile as to come into close approximation. These structures are firmly tethered and consequently this form of gastric volvulus is much less common. Despite the profuse gastric arterial supply, either type of volvulus may compromise the vascularity of the stomach.

GASTRIC SURFACES

When the stomach is empty and contracted, the two surfaces tend to lie facing almost superiorly and inferiorly, but with increasing degrees of distension they come to face progressively more anteriorly and posteriorly.

Anterior (superior) surface

The lateral part of the anterior surface is posterior to the left costal margin and in contact with the diaphragm, which separates it from the left pleura, the base of the left lung, the pericardium and the left sixth to ninth ribs (Fig. 2). It lies posterior to the costal attachments of the upper fibres of transversus abdominis, which separate it from the seventh to ninth costal cartilages. The upper and left part of this surface curves posterolaterally and is in contact with the gastric surface of the spleen. The right half of the anterior surface is related to the left and quadrate lobes of the liver and the anterior abdominal wall. When the stomach is empty, the transverse colon may lie adjacent to the anterior surface. The entire anterior (superior) surface is covered by peritoneum.

Posterior (inferior) surface

Figure 2 Anterior relations of the stomach, viewed from behind

The posterior surface lies anterior to the left crus and lower fibres of the diaphragm, the left inferior phrenic vessels, the left suprarenal gland, the superior pole of the left kidney, the splenic artery, the anterior pancreatic surface, the splenic flexure of the colon and the upper layer of the transverse mesocolon (Fig. 3). Together these form the shallow stomach bed: they are separated from the stomach by the lesser sac (over which the stomach slides as it distends). The upper left part of the surface curves anterolaterally and lies in contact with the gastric surface of the spleen. The greater omentum and the transverse mesocolon separate the stomach from the duodenojejunal flexure and ileum. The posterior surface is covered by peritoneum, except near the cardiac orifice, where a small, triangular area contacts the left diaphragmaticcrus and sometimes the left suprarenal gland. The left gastric vessels reach the lesser curvature at the right extremity of this bare area in the left gastropancreatic fold. The gastrophrenic ligament passes from the lateral aspect of this bare area to the inferior surface of the diaphragm.

GASTRIC ORIFICES

CARDIAC ORIFICE AND GASTRO-OESOPHAGEAL JUNCTION

The opening from the oesophagus into the stomach is the cardiac orifice (Fig. 4). It is typically situated to the left of the midline behind the seventh costal cartilage at the level of the eleventh thoracic vertebra. It is c.10 cm from the anterior abdominal wall and 40 cm from the incisor teeth. The short abdominal part of the oesophagus curves sharply to the left as it descends and is continuous with the cardiac orifice. The right side of the oesophagus is continuous with the lesser curvature, the left side with the greater curvature. There is no specific anatomical cardiac sphincter related to the orifice.

Internally, the transition between oesophagus and stomach is difficult to define because mucosa of gastric fundal pattern extends a variable distance up into the abdominal oesophagus. It usually forms a 'zig-zag' squamo-columnar epithelial junction with the oesophageal epithelium above this Z line (p. 1152). This is often referred to as the gastro-oesophageal junction, for histological and endoscopic purposes. A sling of longitudinal gastric muscle forms a loop on the superior, left, side of the gastro-oesophageal junction between the oesophagus and the lesser curvature, and this is taken as the external boundary of this junction.

GASTRO-OESOPHAGEAL REFLUX

Figure 3 Posterior relations of the stomach.

Figure 4 The valve-like structure formed by the angle of the wall at the cardiac orifice. (Provided by Donald E Low, Department of Surgery, Virginia Mason, Seattle, USA.)

Reflux of gastric contents into the abdominal and lower thoracic oesophagus as a result of transient relaxation of the lower oesophageal sphincter occurs as a normal event in most individuals for a small percentage of their daily life. It also occurs as a result of a weak lower oesophageal sphincter, or of hiatus hernia which disrupts the normal anatomical barriers (p. 1083). Several anatomical and physiological factors normally prevent gastro-oesophageal reflux. The folds of gastric mucosa present in the gastro-oesophageal junction, the mucosal rosette, contribute to the formation of a fluid-and gas-tight seal. They also help to ensure that even low levels of tone within the lower oesophageal wall muscles may occlude the lumen of the junction against low pressures of gastric gas. The angle of the cardiac orifice may help to form a type of 'flap valve' and the length of abdominal oesophagus is buttressed externally by pads of adipose connective tissue at and below the level of the diaphragmatic hiatus. However, the major anti-reflux mechanism is the tonic contractions of the lower oesophageal musculature, which forms an effective high pressure zone (HPZ) (p. 986). The specialized smooth muscle of the wall of the lower oesophagus and the encircling fibres of the crural diaphragm exert a radial pressure that can be measured by a sensing device as it is withdrawn from the stomach into the oesophagus (Paterson 2001). If reflux is to be prevented, this pressure must always exceed the difference between the pressures on either side of the junction, i.e. the difference between intra-abdominal pressure (transferred to the stomach, and augmented by any contraction of the stomach wall itself), and intrathoracic pressure (transferred to the oesophagus).

During expiration, pressure exerted by tonic contraction of the smooth muscle of the lower oesophagus is normally sufficient to oppose the gastro-oesophageal pressure gradient. During inspiration, intra-abdominal pressure rises and intrathoracic pressure becomes more negative, increasing the risk of reflux. This tendency is opposed by additional pressure exerted by contraction of the crural fibres of the diaphragm. (Activation of the crural diaphragm slightly before the costal diaphragm would ensure that contraction of peri-oesophageal fibres preceded the increase in gastro-oesophageal pressure gradient.) The anti-reflux barrier must of course be lowered for swallowing and vomiting. Swallowing is followed immediately by expiration, which relaxes the crural fibres and allows the oesophageal contents to be transferred to the stomach by peristaltic movement. Vomiting is produced by bursts of activity involving co-contraction of the diaphragm, intercostal and abdominal muscles in a pattern distinct from that of respiration: this activity is coordinated with relaxation of the crural fibres around the oesophagus (Miller, 1990).

Barrett's oesophagus

The squamous epithelium lining the lower oesophagus may be pathologically replaced by a columnar, gastric type epithelium. This may occur as islands, strips, or circumferentially, and may extend for a variable length up the lower oesophagus. This process is most likely to be the result of the chronic reflux of gastric contents, acid or alkali, into the oesophagus with a resultant change in mucosal cell type. The abnormal columnar type epithelium present in the anatomical oesophagus is referred to as Barrett's epithelium.

PYLORIC ORIFICE

The pyloric orifice is the opening into the duodenum. The circular pyloric constriction on the surface of the stomach usually indicates the location of the pyloric sphincter and is often marked by a prepyloric vein crossing the anterior surface vertically downwards. The pyloric orifice typically lies 1-2 cm to the right of the midline in the transpyloric plane with the body supine and the stomach empty. The pyloric sphincter is a muscular ring formed by a marked thickening of the circular gastric muscle interlaced with some longitudinal fibres.

GASTRIC FORM AND INTERNAL APPEARANCES

It is clear from contrast radiographic studies that the form and position of the stomach are extremely variable depending on posture, the volume of its contents, and the surrounding viscera. They are also influenced by the tone of the abdominal wall and gastric musculature and by the build of the individual. The empty stomach is most commonly J-shaped and, in the erect posture, the pylorus descends to the level of the second or the third lumbar vertebra. The lowest part of the antrum often lies below the level of the umbilicus. The fundus usually contains gas. The overall axis of the organ is, therefore, slightly inclined from the vertical (Figs 5, 6). In short, obese individuals the axis of the stomach lies more towards the horizontal as a 'steer-horn' shape.

Variation caused by the contents of the stomach mainly affects the body because the pyloric part usually remains contracted during digestion. As the stomach fills, it expands forwards and downwards but, when the colon or small bowel is distended, the fundus enlarges towards the liver and diaphragm. As stomach capacity increases, the pylorus is displaced to the right and the axis of the whole organ lies in a more oblique direction (Figs 5, 7). In this position the anterior and posterior surfaces tend to face forwards and backwards and the lowest part is the pyloric antrum, which extends below the umbilicus. When intestinal distension interferes with downward expansion of the body, the stomach retains a horizontal position.

Figure 5 Axes of the empty and full stomach. As the stomach distends, the greater curvature 'rolls' downwards and the anterosuperior surface comes to lie almost completely vertical as the anterior surface.

During endoscopic examination (Fig. 6), the stomach is typically at least partially distended by air. The cardiac orifice and the lowest portion of the abdominal oesophagus viewed from above are typically closed at rest by tonic contraction of the lower oesophageal musculature. The gastric mucosa lining the orifice is puckered into ridges. It is present for a short but variable distance into the abdominal oesophagus and the transition between columnar and squamous epithelium is usually clearly visible. The presence of abnormal columnar epithelium within the anatomical oesophagus is referred to as Barrett's oesophagus but the precise definition of this condition is difficult. From within the distended stomach, the cardiac orifice appears in the medial wall of the fundus and is asymmetrical. The medial edge of the cardiac orifice is continuous with the medial wall of the body of the stomach. The mucosa is slightly thickened at this point with a raised profile, forming part of the 'mucosal rosette' that lines the orifice. The 'rosette' aids closure of the cardiac orifice and helps prevent reflux of stomach contents into the oesophagus. The medial edge of the orifice is more clearly visible than the lateral edge as it forms a more acute angle with the mucosal lining of the abdominal oesophagus.

Figure 6 Endoscopic appearance of the stomach: A, cardiac orifice from below; B, body greater curvature; C, body lesser curvature; D, pylorus.

In the partly distended stomach, the mucosa of the fundus is thrown into gentle folds with no particular pattern. As the stomach fills towards capacity, however, these folds rapidly become less pronounced, and the wall is nearly smooth when the stomach is over-inflated. The body of the stomach has the most pronounced mucosal folds. Even in moderate distension, they appear as long, broad mucosal ridges running in sinuous strips from fundus to pyloric antrum (Fig. 7). They are seen on all mucosal surfaces of the body but are most obvious on the anterolateral, lateral and posterolateral parts (which correspond to the inner surface of the anterior and posterior external surfaces and to the greater curvature). Here they are occasionally called the magenstrasse, a reference to their possible role in directing liquid entering the stomach immediately down into the pyloric antrum. These folds are least prominent on the medial surface (corresponding to the inner surface of the lesser curvature), which is much smoother, particularly when the stomach distends.

The areae gastricae within the antrum are small nodular elevations of the mucosal surface that are readily seen on double contrast barium meal (Fig. 7). The few folds present in the antrum when the stomach is relaxed disappear with distension. The antrum adjacent to the pyloric canal, the prepyloric antrum, has a smooth mucosal surface culminating in a slight puckering of the mucosa at the pyloric orifice caused by the contraction of the pyloric sphincter.

Figure 7 Double contrast barium meal in the erect position the stomach has a more 'J'-shaped configuration

GASTROSTOMY

Since the lower body and antrum of the stomach is related to the posterior aspect of the left anterior abdominal wall, it may usefully be accessed to form a gastrostomy. Its mobility enables the anterior surface of the stomach to be readily approximated to the parietal peritoneum on the posterior surface of the abdominal wall and a communication to be established between the lumen of the stomach and the surface of the skin. Although this may be performed as a direct open surgical procedure under general anaesthetic it is much more commonly performed using a percutaneous puncture guided by either endoscopic visualization of the stomach or radiological imaging. The procedure is made easier by the fact that the anterior surface of the stomach lies most nearly in the vertical plane when the stomach is distended. One of the main hazards of the procedure results from the occasional interposition of the transverse colon between the stomach and anterior abdominal wall. This may lead to inadvertent transfixion of the colon by the needle puncture system. The variable length of the transverse colonic mesentery means that it may sometimes lie adjacent to the anterior gastric surface when a subject is recumbent. These risks may be reduced by radiological guidance.

To be Continued... (The Vascular, Lymphatic and Innervation)

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