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f. Clinical manifestationg. Classificationh. Pemeriksaan penunjangi. Treatment

j. complicationSTEP 3

1. Why the patient came with the puffy face?Puffy Face

Swollen or puffy face may be normal if you develop it occasionally or once in a blue moon

(requiring no medical work-up) however, if you are experiencing frequent episodes of facial

puffiness, you should seek immediate medical intervention as it may be a sign of a graveunderlying pathology that must be corrected. You should also observe if your family

members or siblings had/ have a history of facial puffiness after waking up in the morning.

Symptoms of Puffy Face

Knowing associated symptoms of puffy face are helpful in diagnosing the primary etiological

event that has led to the development of puffy face. The associated symptoms of facial

puffiness respond very well to lifestyle modification and home remedies to restore the

natural healthy look on your face.

1. Mild Symptoms

Mild symptoms that are associated with puffy face includes pain, redness of entire face or

localized redness at or around eyes, nose or upper/ lower face. In addition, facial puffiness

may also be associated with hives, rashes, bumps or localized lesions. Other mild symptoms

include low grade or high grade fever, nausea and sneezing.

2. Severe Symptoms

Severe symptoms that are associated with facial puffiness warrant emergent medical

attention to prevent life threatening consequences. These symptoms include swelling of

throat that may lead to difficulty with swallowing or breathing, swelling of tongue that

increases the risk of sudden death due to angioedema and obstruction of respiratory

passageways, swelling of nostrils and other vital structures that are associated with

breathing.

Causes of Puffy Face

There are a number of causes that may present as puffy face. Few popular ones are listed as

under:


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1. Dehydration

One of the most common causes of facial puffiness is dehydration. In situations when the

total body intake of water is low, the kidneys conserve water by increasing the absorption of

water that is stored in soft tissues. Moderate dehydration leads to puffiness of face inaddition to swelling of feet and hands. The puffiness of face due to dehydration responds

very well to water intake.

2. Dietary Factor

Certain foods and nutrients significantly increase the risk of developing temporary puffy

face. This includes fatty foods or beverages that dehydrate your body like coffee and tea. In

addition to dehydration, deficiency of vitamin C also presents with puffy face and responds

to supplemental vitamin C and water- melon juice. If you consume alcohol in moderate

amounts, cutting down intake also helps tremendously.

3. Kidney Diseases

Kidney diseases (or renal failure) may also present with puffy face but in vast majority of

cases, the swelling is more pronounced in the peri-orbital region, hands and feet. Speak to

your healthcare provider if you are also experiencing urinary symptoms that points to a

renal pathology.

4. Hypothyroidism

Hormonal disorders are yet another common cause of puffy face due to alteration in the

normal metabolic pathways. In addition to puffy face, you will also have other symptoms of

hypothyroidism like weight gain, constipation, dryness of skin and changes in the rhythm of

heart.

5. Cushing's Syndrome

Cushings syndrome is marked by high cortisol levels that alter normal vascular metabolism

and leads to a round moon-shaped puffy due to deposition of fat. It may be a result of

endogenous hyper-secretion of cortisol or exogenous intake of steroids to relieve chronic

inflammatory conditions like arthritis, asthma or other similar ailments.

6. Other Causes

Other uncommon conditions that may also present with puffy face includes obesity, insect

bite, allergic reaction to drugs or certain foods, angioedema, abscess or infection of tooth,

sinuses or associated structures of head and neck region, nephritic or nephrotic syndrome,

mumps and swelling of salivary glands (like inflammation of parotid gland).


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Relieves for Puffy Face

1. Dietary Methods

Dietary modifications are helpful in relieving puffiness of face without requiring any other

intervention.

Maintain high hydration status by increasing your water intake to at least 2 liters perday.

Salt osmotically attracts water and aggravates the symptoms of edema. Limiting yoursalt intake is extremely helpful if you have puffy face due to renal problem or

hypertension.

High alcohol intake is associated with dieresis (excretion of large amounts of water inurine).

Eat Healthy and balanced diet that is rich in quality vitamins and minerals.2. Regular Exercises

Perform regular physical activity since sometimes the inflammatory reactions block

lymphatics leading to puffiness of face. With regular physical therapy and simple stretching

exercises you can relieve edematous swelling of the face and other parts of the body.

3. Homemade Remedies

Home remedies are helpful in alleviating the symptoms of puffy face. You can try these

remedies for speedy recovery:

Cold Milk. In situations when the swelling on your face is due to an abscess or sore,application of cold milk with cotton ball is helpful in reducing the pain, swelling and

inflammation by acting as a cleansing agent. Moreover, also wash your face throughout

the day with cold water (without any soap).

Cold Creams and Lotions. You can also store your creams and lotions in refrigerator(especially in hot humid days) to alleviate puffiness of face.

Cold Compress. Cold compresses are helpful if you have developed an inflammatory orpainful swelling due to trauma or underlying inflammation (abscess)

4. Sleeping Position

Changing your sleeping position also helps a great deal. Using higher pillows usually helps in

reducing edema of face due to abnormal posture. However, caution must be maintained

since high pillows or higher head support may also lead to neck-pain, insomnia or breathing

difficulties.

5. Medications

Depending upon the cause of puffy face, your healthcare provider may advise youantibiotics or anti-viral medications to relieve the symptoms due to bacterial or viral


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4. Why the man facial anhidrosis, miosis and ptosis?Horner syndrome (Horners syndrome) results from an interruption of the sympathetic

nerve supply to the eye and is characterized by the classic triad of miosis (ie, constricted

pupil), partialptosis,and loss of hemifacial sweating (ie, anhidrosis). The term Horner

syndrome is commonly used in English-speaking countries, whereas the term Bernard-Horner syndrome is common in France. Von Passow syndrome is an association of Horner

syndrome with iris heterochromia (heterochromia iridis).[1]

Causes of Horner syndrome include the following:

Lesion of the primary neuron Brainstem stroke or tumor or syrinx of the preganglionic neuronIn one study, 33% of

patients with brainstem lesions demonstrated Horner syndrome[2]

Trauma to the brachial plexus Tumors (eg,Pancoast)or infection of the lung apex Lesion of the postganglionic neuron Dissecting carotid aneurysmIn one study, 44% (65/146) of patients with internal

extracranial carotid artery dissections had painful Horner syndrome, which remained

isolated in half the cases (32/65)[3]

Carotid artery ischemia Migraine Middle cranial fossa neoplasm

Horner syndrome is uncommon. No age, sexual, or racial predilections are known to exist.

The prognosis and the complications to be expected depend on the underlying cause of the

syndrome, as does treatment.

Anatomy

Sympathetic innervation to the eye consists of a 3-neuron arc. First-order central

sympathetic fibers arise from the posterolateral hypothalamus, descend uncrossed through

the midbrain and pons, and terminate in the intermediolateral cell column of the spinal cord

at the level of C8-T2 (ciliospinal center of Budge). Second-order preganglionic pupillomotor

fibers exit the spinal cord at the level of T1 and enter the cervical sympathetic chain, where

they are in close proximity to the pulmonary apex and the subclavian artery.

The fibers ascend through the sympathetic chain and synapse in the superior cervicalganglion at the level of the bifurcation of the common carotid artery (C3-C4). Postganglionic

pupillomotor fibers exit the superior cervical ganglion and ascend along the internal carotid

artery. Shortly after the postganglionic fibers leave the superior cervical ganglion,

vasomotor and sudomotor fibers branch off, traveling along the external carotid artery to

innervate the blood vessels and sweat glands of the face.

The third-order pupillomotor fibers ascending along the internal carotid artery enter the

cavernous sinus. The fibers then leave the carotid plexus briefly to join the abducens nerve

(cranial nerve [CN] VI) in the cavernous sinus and enter the orbit through the superior

orbital fissure along with the ophthalmic branch (V1) of the trigeminal nerve (CN V) via the

long ciliary nerves. The long ciliary nerves then innervate the iris dilator and the Mllermuscle.
http://emedicine.medscape.com/article/1212082-overviewhttp://emedicine.medscape.com/article/1212082-overviewhttp://emedicine.medscape.com/article/1212082-overviewhttp://emedicine.medscape.com/article/284011-overviewhttp://emedicine.medscape.com/article/284011-overviewhttp://emedicine.medscape.com/article/284011-overviewhttp://emedicine.medscape.com/article/1142556-overviewhttp://emedicine.medscape.com/article/1142556-overviewhttp://emedicine.medscape.com/article/1142556-overviewhttp://emedicine.medscape.com/article/284011-overviewhttp://emedicine.medscape.com/article/1212082-overview


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Pathophysiology

Horner syndrome may develop from lesions at any point along the sympathetic

pathway.[4]

Abnormalities found in all patients, regardless of the level of interruption,

include the following:

Mild-to-moderate ptosis, owing to denervation of the sympathetically controlled Mllermuscle

Slight elevation of the lower lid (upside-down ptosis), owing to denervation of the lower lidmuscle (analogous to the denervation of the Mller muscle in the upper lid)

Miosis and dilation lag, where pupillary dilation after psychosensory stimuli is slower in theaffected pupil than in the unaffected pupil

Depending on the level of the lesion, impaired flushing and sweating may be found

ipsilaterally. With central first-order neuron lesions, anhidrosis affects the ipsilateral side of

the body. Lesions affecting second-order neurons may cause anhidrosis of the ipsilateralface. With postganglionic lesions occurring after vasomotor and sudomotor fibers have

branched off the sympathetic chain, anhidrosis is either absent or limited to an area above

the ipsilateral brow. The pupils react normally to light and accommodation.

Iris heterochromia (with the affected eye being hypopigmented) is seen in congenital

Horner syndrome or Horner syndrome that occurs in children younger than 2 years. Iris

heterochromia also may occur in long-standing Horner syndrome.

Etiology

Horner syndrome can be congenital, acquired, or purely hereditary (autosomal dominant).

The interruption of the sympathetic fibers may occur centrally (ie, between thehypothalamus and the fibers point of exit from the spinal cord *C8 to T2+) or peripherally

(ie, in cervical sympathetic chain, at the superior cervical ganglion, or along the carotid

artery).

The common lesions that cause Horner syndrome interfere with preganglionic fibers as they

course through the upper thorax. Virtually all lesions producing postganglionic sympathetic

dysfunction are located intracranially or intraorbitally because the superior cervical ganglion

is near the skull. Preganglionic Horner syndrome indicates a serious underlying pathology

and is associated with a high incidence of malignancy. Postganglionic involvement has

primarily benign causes (ie, usually a vascular headache).

Causes of Horner syndrome may also be classified as involving first-order, second-order, or

third-order neuron lesions. First-order neuron lesions that may give rise to the syndrome

include the following:

Arnold-Chiari malformation Basal meningitis (eg, syphilis) Basal skull tumors Cerebral vascular accident (CVA)/Wallenberg syndrome (lateral medullary syndrome) Demyelinating disease (eg, multiple sclerosis) Lesions in the hypothalamus or medulla Intrapontine hemorrhage


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Neck trauma (eg, traumatic dislocation of cervical vertebrae or traumatic dissection of thevertebral artery) - Horner syndrome occurring in association withspinal cord

traumasuggests a high cervical cord lesion because it does not occur with lesions below T2

or T3

Pituitary tumor Syringomyelia

Second-order neuron lesions that may give rise to Horner syndrome include the following:

Pancoast tumor (tumor in the apex of the lung, most commonly squamous cell carcinoma) Birth trauma with injury to lower brachial plexus Cervical rib Aneurysm or dissection of the aorta Lesions of the subclavian or common carotid artery Central venous catheterization Trauma or surgical injury (eg, from radical neck dissection, thyroidectomy, carotid

angiography, or coronary artery bypass grafting) Chest tubes Lymphadenopathy (eg, Hodgkin disease, leukemia, tuberculosis, or mediastinal tumors) Mandibular tooth abscess Lesions of the middle ear (eg, acute otitis media) Neuroblastoma[5]

Third-order neuron lesions that may give rise to Horner syndrome include the following:

Internal carotid artery dissection (associated with sudden ipsilateral face or neck pain)[6] Raeder syndrome (paratrigeminal syndrome) - Oculosympathetic paresis and ipsilateral

facial pain with variable involvement of the trigeminal and oculomotor nerves

Carotid cavernous fistula Cluster or migraine headache Herpes zoster

Drugs that may cause symptoms similar to Horner syndrome include the following:

Acetophenazine Alseroxylon Bupivacaine Butaperazine Carphenazine Chloroprocaine Chlorpromazine Deserpidine Diacetylmorphine Diethazine Ethopropazine Etidocaine Fluphenazine Guanethidine Influenza virus vaccine Levodopa Lidocaine Mepivacaine
http://emedicine.medscape.com/article/1149070-overviewhttp://emedicine.medscape.com/article/1149070-overviewhttp://emedicine.medscape.com/article/1149070-overviewhttp://emedicine.medscape.com/article/1149070-overviewhttp://emedicine.medscape.com/article/1151685-overviewhttp://emedicine.medscape.com/article/1151685-overviewhttp://emedicine.medscape.com/article/1151685-overviewhttp://emedicine.medscape.com/article/1149070-overviewhttp://emedicine.medscape.com/article/1149070-overview


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Mesoridazine Methdilazine Methotrimeprazine Oral contraceptives Perazine Prilocaine Procaine Prochlorperazine Promazine Promethazine Propoxycaine Reserpine Thioproperazine Thioridazine Trifluoperazine

Differential Diagnosis

Horner syndrome in the presence of pain merits special consideration.

Horner syndrome in the presence of axial, shoulder, scapula, arm, or hand pain may be

indicative of compression by an apical lung tumor (Pancoast tumor).

Horner syndrome in the presence of acute-onset, ipsilateral facial or neck pain may indicate

carotid artery dissection, which may be caused by cardiovascular disease, arteriopathy (eg,

fibromuscular dysplasia or collagen disorders), or trauma (even minor trauma, such as

results from quick head turns). If carotid artery dissection is suspected, especially if thereare signs or symptoms of retinal ischemia, urgent neuroimaging studies (magnetic

resonance imaging or magnetic resonance angiography) should be obtained along with

neurologic consultation.

Postganglionic Horner syndrome associated with ipsilateral headache has several causes.

Patients with spontaneous carotid artery dissection may present with Horner syndrome and

ipsilateral headache. Patients with cluster headaches may develop ipsilateral Horner

syndrome during an acute attack.

The term Raeder paratrigeminal syndrome is applied to patients, usually middle-aged males,

who have Horner syndrome and daily unilateral head pain. In the original Raeder syndrome,the pain is trigeminal pain associated with hypoesthesia or anesthesia in the distribution of

the trigeminal nerve (cranial nerve [CN] V). Pain related to Raeder syndrome can be

distinguished from that related to cluster headaches or carotid disease in that the latter

conditions occur without impairment of trigeminal nerve function.

Horner syndrome may be the first manifestation of neuroblastoma.

Conditions to be considered in the differential diagnosis include the following:

Adie pupil Anisocoria Argyll Robertson pupil
http://emedicine.medscape.com/article/1158571-overviewhttp://emedicine.medscape.com/article/1158571-overviewhttp://emedicine.medscape.com/article/1158571-overview


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Holmes-Adie pupil (contralateral) Iris sphincter muscle damage Senile miosis Third nerve palsy Unilateral use of miotic drugs Unilateral use of mydriatic drugs

Laboratory Studies

In general, laboratory studies do not play a significant role in the diagnosis and management

of Horner syndrome. However, depending on the localization and suspected etiology,

certain laboratory tests may be considered, in conjunction with appropriate medical

consultation. These include the following:

Complete blood count (CBC) Fluorescent treponemal antibody absorption (FTA-ABS) test Venereal Disease Research Laboratory (VDRL) test Purified protein derivative (PPD) placement Urine test (ie, vanillylmandelic acid [VMA] and homovanillic acid [HVA]) to rule out

neuroblastoma

Imaging Studies

Imaging studies may be ordered in conjunction with appropriate medical or surgical

consultation, depending on the localization and suspected etiology.[14]

A chest radiograph should be obtained; apical bronchogenic carcinoma is the most common

cause of Horner syndrome. If stroke is suspected, computed tomography (CT) of the head

should be performed.

Painful Horner syndrome should alert the physician to the possibility of carotid artery

dissection, and the patient should undergo further testing (ie, magnetic resonance imaging

[MRI]/magnetic resonance angiography [MRA] of the brain and neck) to exclude this

possibility. Internal carotid artery dissection is life-threatening and carries a risk that the

patient will experience a disabling stroke.

Ultrasonography may be considered but has not been found to be reliable for diagnosing

carotid artery dissection in patients with isolated Horner syndrome.

http://emedicine.medscape.com/article/1220091-overview#aw2aab6b9

Horner syndrome

Key pointsHorner syndrome is characterized clinically by miosis, ptosis, and anhidrosis.The lesion is due to disruption of the oculosympathetic pathway.Carotid dissection is a potentially life-threatening acute etiology.Pharmacologic testing with cocaine or apraclonidine can confirm the clinical

diagnosis of Horner syndrome.

Imaging of the entire oculosympathetic axis may be indicated in the evaluation of

Horner syndrome.
http://emedicine.medscape.com/article/1220091-overview#aw2aab6b9http://emedicine.medscape.com/article/1220091-overview#aw2aab6b9http://emedicine.medscape.com/article/1220091-overview#aw2aab6b9


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Historical note and nomenclatureThe syndrome of ptosis, miosis, and anhidrosis due to a lesion in the sympathetic

pathway to the eye is known commonly as Horner syndrome. Johann Friedrich Hornerwas a talented and well-respected 19th-century Swiss ophthalmologist. In 1869, hedescribed a 40-year-old woman with headaches who had a right droopy eyelid,

smaller right pupil, and right facial flushing. He attributed the findings to damage ofthe cervical sympathetic nerves to the eye. Although his case was not the first toreport the clinical effects of damage to the cervical sympathetic nerves, his name hasbecome an eponym for the triad of ptosis, miosis, andanhydrosis.Professor Horner is

also remembered as the founder of Swiss ophthalmology. Because the Frenchphysiologist Claude Bernard described the signs of sympathetic injury in animals 17years earlier in 1852, the syndrome is also called Bernard-Horner syndrome in someparts of the world(Pearce 1995).

Clinical manifestationsHorner syndrome is caused by a lesion of the sympathetic pathway supplying the

head, eye, and neck.

Ptosis.There is both upper and lower lid ptosis due to loss of sympatheticinnervation to the superior and inferior tarsal muscles. The upper lid ptosis is usuallymild and can be voluntarily overcome if the patient utilizes the levator palpebrae andfrontalis muscles excessively as these are not innervated by the oculosympatheticnerves. One way to check for lower lid ptosis is to ask the patient to look upwardslightly. In the eye with an oculosympathetic defect, the inferior corneal margin abutsthe lower lid margin (upside down ptosis). In the normal eye, sclera is visible between

the inferior corneal limbus and the lower lid margin. This lower lid ptosis is also knownas "reverse" or "upside-down ptosis."Apparent enophthalmos.In the relaxed state, the combined upper and lower lid

ptosis narrows the palpebral fissure and creates the false impression of

enophthalmos(Thompson 1977;Miller 1985).Measurement with anexophthalmometer reveals the enophthalmos to be apparent only.

Miosis.The anisocoria of a Horner syndrome is generally small, about 1.0 mm orless. The miosis (smaller pupil) results from a lack of an active pupillodilator due to anoculosympathetic defect; therefore, the anisocoria is greater in darkness than in roomlight. In ambient room light conditions, the anisocoria can be clinically inapparent ifthe parasympathetic pupilloconstrictor activity overshadows the unequal sympathetic

pupillodilator activity between the 2 eyes. Therefore, it is important to always checkthe pupils in room light and in darkness as well as with added light.Dilation lag.A normal pupil will dilate promptly within 5 seconds after the light is

turned off. This is chiefly due to sympathetic activation of the pupillodilator that

"pulls" the pupil open. However, a Horner pupil lacks this activity and dilates slowly,over 15 to 20 seconds, from parasympathetic inhibition "letting go" of thepupilloconstrictor(Lowenstein and Loewenfeld 1950).Because the pupils need to be

observed simultaneously in the dark, a camera with infrared viewing greatly facilitatesthe examination for dilation lag.Clinical photographs of the pupil may be useful for documentation of dilation lag.

Using a flash Polaroid or digital camera, the decreasing anisocoria between 5 and 15seconds in darkness can be easily recorded with static photographs. Finding a change(decrease) in anisocoria of 0.4 mm or more between 5 and 15 seconds after a lightflash is 100% specific for Horner syndrome, but unfortunately, not all Horner patients

demonstrate this finding(Kawasaki and Kardon 2004).Drowsiness causes miosis andobscures dilation lag, so arouse the patient before testing. The dilation lag may alsoonly be intermittently present, and the absence of the dilation lag does not rule outHorner syndrome(Crippa et al 2007).In the clinically suspect patient, pharmacologic

testing must be pursued.

When a patient is suspected of having a bilateral Horner syndrome, asymmetry ofpupillary dilation and pharmacologic responsiveness can no longer be used fordiagnostic purposes. Infrared computerized pupillography has been utilized to define
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8. What are the DD?


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Sumber : Aplikasi Klinis Patofisiologi Valentina L. Brashers


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Sumber : Keperawatan Medikal Bedah Oleh Niluh Gede Yasmin Asih, Christantie Effendy


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Sumber : Buku Saku Patofisiologi Corwin Oleh Elizabeth J. Corwin


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STEP 4

Zat karsinogenik

Terhirup (inhalan)

Massatumor

Menekan saraf

sympatis

miosis

ptosis

anhidrosis

Horners Syndrom

Menyebar ke paru

Mengganggu

pertumbuh sel

berlebihan

Radiologi

Opaq massManifest

Loss appetiteFever

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