Prostatitis + Hemorrhoids = Misery
Thad Noles
hemorrhoids on top of my prostatitis. Truly, this is miserable. At any rate,
I attempted to use Preparation H to provide symptomatic relief. After having
used it for about a day, I noticed some "strange feelings" in my prostate.
Not really pain but nonetheless irritating.
I remembered a few posts on this newsgroup about using witch hazel for
hemorrhoids and I was curious if Preparation H contained it. As I read the
active ingredients of Preparation H, I noticed to my horror that it contains
Phenlyephrine HCL 0.25% along with the standard "Do not use this product if
you have difficulty in urination due to enlargement of the prostate gland."
This is the same type of substance that caused my prostatitis in the first
place (as far as I can tell), and it too had that same warning. I
immediately ran to the bathroom to wash it off. I expected a flare up any
second (and am still praying that I am overreacting).
At any rate, here's my question. Does anyone know about using witch hazel
for the treatment of hemorrhoids? And more importantly, do you think witch
hazel could cause a problem in someone with prostatitis? Any help with this
would be greatly appreciated.
JORDAN DIMITRAKOV, MD, PhD
>In accordance with Murphy's Law, it seems I have now developed a case of
>hemorrhoids on top of my prostatitis. Truly, this is miserable. At any rate,
>I attempted to use Preparation H to provide symptomatic relief. After having
>used it for about a day, I noticed some "strange feelings" in my prostate.
>Not really pain but nonetheless irritating.
>
>I remembered a few posts on this newsgroup about using witch hazel for
>hemorrhoids and I was curious if Preparation H contained it. As I read the
>active ingredients of Preparation H, I noticed to my horror that it contains
>Phenlyephrine HCL 0.25% along with the standard "Do not use this product if
>you have difficulty in urination due to enlargement of the prostate gland."
>This is the same type of substance that caused my prostatitis in the first
>place (as far as I can tell), and it too had that same warning. I
>immediately ran to the bathroom to wash it off. I expected a flare up any
>second (and am still praying that I am overreacting).
>
>At any rate, here's my question. Does anyone know about using witch hazel
>for the treatment of hemorrhoids?
Blumenthal: The Complete German Commission E Monographs: Therapeutic Guide
to
Herbal Medicines, First Edition, Copyright © 1998 American Botanical Council
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Witch Hazel leaf and bark
Hamamelidis folium et cortex
Hamamelisbla tter und-rinde
Published August 21, 1985; Revised March 13, 1990
Name of Drug
Hamamelidis folium, witch hazel leaf.
Hamamelidis cortex, witch hazel bark.
Composition of Drug
Witch hazel leaf consists of the dried leaf of Hamamelis virginiana L. [Fam.
Hamamelidaceae], as well as its preparations in effective dosage.
The drug contains 3 - 8 percent tannin, mainly gallotannins. Other
ingredients
are flavonoids and essential oil.
Witch hazel bark consists of the dried bark of the trunk and branches of
H.virginiana L., as well as its preparations in effective dosage.
The drug contains at least 4 percent tannins. Characteristic ingredients of
witch hazel bark are s-hamamelitannin and gamma-hamamelitannin, the depside
ellagitannin, catechin derivatives, and free gallic acid.
Fresh leaf and twigs of H. virginiana L., consists of leaves and twigs
collected in spring and early summer for the production of water
distillates.
Uses
Minor injuries of skin, local inflammation of skin and mucous membranes.
Hemorrhoids. Varicose veins.
Contraindications
None known.
Side Effects
None known.
Interactions with Other Drugs
None known.
Dosage
Unless otherwise prescribed:
External:
Water steam distillate (witch hazel water) undiluted or diluted 1:3with
water;
For poultices, 20 - 30 percent insemi-solid preparations.
Extract preparations:Semi-solid and liquid preparations,corresponding to 5 -
10 percent drug.
Drug:Decoctions of 5 - 10 g of herb per cup (250 ml) of water for compresses
and irrigations.
Internal use (mucous membranes):
Suppositories:1 - 3 times daily, the amount of a preparation corresponding
to
0.1 - 1 g drug to be applied 1 - 3 times a day.
Other preparations:Several times daily, correspondingto 0.1 - 1 g drug in
preparations, or witch hazel water undiluted or diluted with water.
Mode of Administration
Witch hazel leaves and bark:
Cut drug or extracts for internal and external use.
Fresh leaves and bark of Hamamelis:
Steam distillate for internal and external use.
Actions
Astringent
Antiinflammatory
Locally hemostatic
And some more:
Primary Care; Clinics in Office Practice
Volume 26 • Number 1 • March 1999
OFFICE MANAGEMENT OF COMMON ANORECTAL PROBLEMS
ANORECTAL PAIN AND IRRITATION
Anal Fissure, Levator Syndrome, Proctalgia Fugax, and Pruritis Ani
Chris Vincent MD
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Department of Family Medicine, Swedish Family Practice Residency, University
of Washington School of Medicine, Seattle, Washington
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Address reprint requests to
Chris Vincent, MD
Swedish Family Practice Residency
Swedish Family Medicine
1401 Madison, Suite 100
Seattle, WA 98104
e-mail: cvin...@u.washington.edu
Most patients with anal pain or irritation present to their physicians
complaining of hemorrhoids. [43] [51] Many, however, turn out to have
another
reason for their discomfort. Anal fissures, proctalgia fugax, levator ani
syndrome, and pruritis ani are common causes of anorectal pain and
irritation.
The primary care clinician can diagnose and manage these diseases with
confidence, as most patients have uncomplicated cases that respond to simple
lifestyle changes and routine medications.
ANAL FISSURES
Definition and Epidemiology
An anal fissure is a longitudinal tear or ulcerated area in the distal anal
canal, usually in the posterior or anterior midline and usually extending
from
the level of the dentate line out to the anal verge. [43] Acute anal
fissures
have little surrounding inflammation and may spontaneously heal in 2 to 3
weeks. A chronic anal fissure usually is deeper and is
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54
associated with secondary changes such as a sentinel tag, hypertrophied anal
papilla, induration of the edge of the fissure, and relative anal stenosis.
[74] The internal anal sphincter muscle fibers may be visible at its base.
Anal fissures affect men and women equally. Most anal fissures occur in the
posterior midline; women are slightly more likely than men to have anterior
fissures (Table 1) . A patient with multiple fissures, or whose fissure is
not
in the midline, is more likely to have an associated colorectal disorder
such
as Crohn's disease. [19] Although anal fissures are seen in both newborns
and
the elderly, 87% of chronic sufferers are between 20 and 60 years old, and
54%
are between 30 and 50. [55] [65]
Cause and Pathophysiology
In the past, clinicians thought that tearing of the anal skin as the patient
passed a hard, dry stool caused anal fissures. In fact, only 25% of patients
with fissures have constipation. [50] Furthermore, this theory did not
explain
why most fissures are in the posterior midline. Klosterhalfen et al, [42] in
their study of the inferior rectal artery anatomy in cadavers, proposed an
alternative hypothesis. They noted that in most subjects, the capillary
system
of the inferior rectal artery ended at the posterior commissure, making this
site prone to ischemic injury. Using laser Doppler flowmetry in healthy
volunteers, Schouten and colleagues [77] confirmed that the blood supply to
the posterior anoderm is lower than at the other sides of the canal.
Furthermore, patients with anal fissures showed improvement in the posterior
commissure blood flow following lateral sphincterotomy. [76] Spasm of the
internal anal sphincter may worsen the ischemia and retard healing. Most
anal
manometric studies show an increase in the resting anal pressure in patients
with anal fissures, a finding consistent with chronic internal anal
sphincter
contraction. [3] [10] [17] [22] [31] [41] [45] [62] [76] [92] Additional
risk
factors for anal fissures include a low fiber diet and previous anal
surgery.
[37]
Diagnosis and Clinical Features
Almost all patients with anal fissures complain of perirectal pain; many
also
have rectal bleeding. In a study of 172 persons with chronic
TABLE 1 -- LOCATION OF ANAL FISSURES
Data from References [47] [55] [65] Gender Fissure Location
Posterior Anterior Other
Male 83%-84% 6%-9% 7%-10%
Female 67%-68% 10%-21% 11%-14%
Both 75%-76% 13%-16% 9%-12%
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55
anal fissures, 86% complained of pain, and 60% had bleeding. [69] The pain
of
anal fissures is sharp, searing, or burning and is associated with
defecation.
[43] [69] The pain may vary from mild to severe, and may last minutes to
hours. [43] [58] Bleeding from anal fissures is bright red and not mixed
with
the stool; it may be noted only on the toilet tissue. Other less common
symptoms include perianal pruritis and mucus drainage. [36] [43] [58] [69]
A gentle and reassuring manner is necessary to examine someone suffering
from
an anal fissure; many patients tolerate only gradual spreading of the
buttocks. The acute anal fissure looks like a superficial tear in the anal
mucosa. A chronic anal fissure is deeper and often has an associated
proximal
anal papilla and distal sentinel tag (Figs. 1 (Figure Not Available) and 2)
.
The fissure margins may be inflamed and fibers of the internal anal
sphincter
may be visible at its base. [36] [43] [58] [74] If the patient has atypical
or
multiple fissures, the practitioner should search for an underlying
disorder.
Causes of atypical or multiple fissures are *
Inflammatory bowel disease
Crohn's disease
Ulcerative colitis
Infections
Tuberculosis
Gonorrhea
Syphilis
Chlamydia
Human Immunodeficiency Virus
Herpes simplex
Cancer
Figure 1. (Figure Not Available) Chronic anal fissure showing: A, External
hemorrhoid. B, Fibers of the internal anal sphincter at the base. C,
Sentinel
tag. (Courtesy of RP Billingham, MD, Seattle, Washington.)
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* Data fromReferences [36] [43] [74]
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56
Figure 2. Coronal section of rectum with a chronic anal fissure showing: A,
Dentate line. B, Anal papilla. C, Fibers of the internal anal sphincter at
the
base. D, Sentinel tag. E, Internal anal sphincter. F, External anal
sphincter.
Anoscopic and digital rectal examinations, although recommended in patients
with chronic anal fissures, may be painful. In these circumstances, an
anesthetic such as 2% lidocaine jelly applied to the fissure may lessen the
examination discomfort. [36] [43]
Treatment and Patient Education
Anal fissure treatment includes dietary manipulation, medication, anal
dilatation, and internal sphincterotomy. [74] Patients with acute anal
fissures who have diarrhea or constipation are told to consume high fiber
foods. Topical anesthetics and corticosteroids often are recommended as
well.
[38] Warm sitz baths may help relieve the pain. These simple measures may
heal
acute anal fissures within 3 weeks in almost 90% of patients.
In contrast to acute anal fissures, only 40% to 60% of patients with chronic
anal fissures improve with conservative therapy. [25] [47] Historically,
anal
dilatation, fissurectomy, or sphincterotomy have been offered to these
patients. Anal dilatation has been employed extensively in Europe and
Australia; however results have been mixed. [25] [35] [56] [68] Many feel
that
anal dilatation is simply an uncontrolled sphincterotomy with a higher
incontinence rate than other therapies. [58] [74] Compared with lateral
internal sphincterotomy, fissurectomy has a lower cure rate and higher
incidence of postoperative pain. Therefore, in most of the world, including
North America, lateral internal sphincterotomy is the procedure of choice.
[43] [51] [58]
Lateral internal sphincterotomy was first described in the 1950s. [15] The
lateral is preferred over the posterior approach as it is less likely to
produce a keyhole deformity, which causes fecal soiling. [43] [61] Notaras
[61] modified the technique in the late 1960s, demonstrating a minimally
invasive
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57
subcutaneous approach that has a high success and low complication rate.
Surgeons continue to refine the operation, so controversy still exists
concerning open versus subcutaneous approach. [21] [30] [46]
Complications of lateral internal sphincterotomy include late healing of the
sphincterotomy site, wound infection, fecal or flatus incontinence, and
fissure recurrence. [30] [46] [50] [86] Although incontinence rates for
flatus
vary from 0% to 35%, and for feces from 0% to 5%, [30] [46] [50] [86] most
researchers report an incontinence rate for flatus that is 2% or less and
for
feces a rate that is 1% or less. Similarly, most surgeons note a long-term
operative failure rate of less than 3%. [46] [50] [58] [86] Because
incontinence may rarely be a problem, the American Society of Colon and
Rectal
Surgeons advises caution before performing lateral internal sphincterotomy
in
patients with diarrhea, irritable bowel syndrome, diabetes, or other
pre-existing states that predispose them to incontinence. [74] This view has
prompted some authors to recommend preoperative anal manometry and endoanal
ultrasound in patients with recurrent fissures and in women with a history
of
episiotomy or third-degree tear during labor. [50] Others regard
preoperative
anal manometry as unnecessary because presurgical and postsurgical
measurement
of the internal anal sphincter resting pressure shows no statistically
significant correlation. [72]
In the last decade, several researchers have successfully treated chronic
anal
fissures with the novel use of two medications: topical nitroglycerin and
injectable botulin toxin. [52] [75] Recently, O'Kelly [63] and others
demonstrated that nitric oxide is the inhibitory neurotransmitter
responsible
for internal anal sphincter relaxation. Loder et al [48] showed that 0.2%
topical nitroglycerin ointment, a nitric oxide donor, produced a 27%
decrease
in mean resting sphincter pressure. Since that 1994 paper, at least six
groups
have published their experiences using nitroglycerin to treat chronic anal
fissures. [5] [24] [49] [64] [83] [88]
Two randomized, controlled trials of nitroglycerin in patients with anal
fissures have been published. [5] [49] Bacher et al [4] noted that after 1
month, 80% of subjects treated with nitroglycerin applied three times daily
to
the anoderm had healed fissures, compared with only 40% who received topical
lidocaine. Similar results were reported in another study in which
nitroglycerin was used twice daily. After 8 weeks, the anal fissure resolved
in 68% of the treatment cohort, compared with 8% of the placebo group. [49]
Compared with placebo, subjects receiving nitroglycerin ointment had a
statistically significant fall in internal anal sphincter resting pressure
and
rise in anodermal blood flow. [5] [49]
All researchers mention a dramatic reduction in anal fissure pain with
nitroglycerin. [5] [24] [49] [64] [83] [88] Complications include headache
in
20% to 35% and occasional tachyphylaxis. [5] [24] [88] Long-term success
rates
are not known, but most patients who relapse respond to retreatment. [49]
Injectable botulin toxin also shows promise as a nonsurgical treatment of
chronic anal fissures. [28] [39] [53] [54] Jost [39] reported fissure
healing
in 79 of 100 patients 6 months after 2.5 to 5 U of botulin toxin was
injected
into the external (not internal) anal sphincter. Seven patients experienced
transitory fecal incontinence. In a double-blind, randomized, controlled
trial
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58
involving 30 subjects, Maria et al [53] compared injections of saline versus
20 U of botulin toxin into the internal anal sphincter. They demonstrated
symptom relief in 87% and fissure closure in 79% of treated patients.
Results
for the placebo group were 27% and 13% respectively; the differences were
statistically significant at the P = 0.003 level. No relapses were noted
during an average follow-up of 16 months.
Most patients with anal fissures respond to conservative treatment such as
stool softeners (if necessary), sitz baths, and daily application of 1%
hydrocortisone cream to the fissure. Patients who fail to improve after 4
weeks should be offered lateral internal sphincterotomy. Topical
nitroglycerin
ointment and injectable botulin toxin are experimental treatments requiring
further study prior to general acceptance. Neither drug is approved by the
Food and Drug Administration for this indication.
PERIRECTAL PAIN SYNDROMES: LEVATOR ANI SYNDROME AND PROCTALGIA FUGAX
Definition and Epidemiology
Proctalgia, or perirectal pain, was first described in the 19th century.
[57]
Three terms are used to classify proctalgia: levator ani (or levator spasm)
syndrome, proctalgia fugax, and coccygodynia. [51] [91] Levator ani syndrome
refers to chronic or recurrent rectal pain or aching, with episodes lasting
20
minutes or longer in the absence of organic disease that could account for
the
pain. [91] Proctalgia fugax connotes anal or rectal pain, lasting for
seconds
to minutes and then disappearing for days to months, in the absence of
organic
disease to account for these symptoms. [91] Coccygodynia usually describes
tenderness of the tip of the coccyx and is synonymous with levator ani
syndrome. Unfortunately, the three terms have been used interchangeably in
the
literature, making precise recommendations for treatment difficult.
Both levator ani syndrome and proctalgia fugax are common disorders. It is
estimated that 6% of the United States population suffers from levator ani
syndrome, while 8% have proctalgia fugax. [12] Proctalgia fugax was at one
time thought to be a disorder of perfectionistic young men. [67] It is now
apparent that both proctalgia fugax and levator ani syndrome occur slightly
more often in women. Both are more common in patients under age 45;
psychological factors are not always present (see below). [12]
Cause and Pathophysiology
Levator Ani Syndrome
Thiele generally is acknowledged as the first to recognize the relationship
between levator ani muscle spasm and chronic intermittent rectal pain. [84]
The levator ani consists of three muscles: the ileococcygeus the
puborectalis,
and pubococcygeus. These three surround the anus to form
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59
a muscular sling that supports the rectum. The muscle is palpated easily
during a digital rectal examination. Chronic tension of the levator muscle
is
thought to cause the pain that characterizes levator ani syndrome. [91]
Proctalgia Fugax
The cause of proctalgia fugax is not known, but current theories favor
rectal
muscle spasm. [4] [60] [91] Anal manometric studies have demonstrated that
patients with proctalgia fugax have normal anorectal muscle function at
rest,
but develop anal smooth muscle dysfunction during a painful attack. [14]
[73]
Two families with hereditary proctalgia fugax have been studied. Members of
both families had endosonographic evidence of thickened internal anal
sphincter muscles. Anal manometry of affected persons showed increased
resting
pressure and prominent ultraslow wave pressure oscillations. The latter were
thought to be caused by smooth muscle contractions of the internal anal
sphincter, and peaks in pressure were associated with characteristic pain.
[9]
[40] Furthermore, drugs known to relax smooth muscles may have relieved
attacks of proctalgia fugax. [7] [13] [29]
Proctalgia fugax may be associated with functional gastrointestinal
disorders.
Abdominal pain and distension, frequent loose stools, and a sensation of
incomplete evacuation after defecation have been noted more often in
patients
with proctalgia fugax. The significance of this remains a mystery. [85]
An investigation of the psychological aspects of proctalgia fugax done in
the
1960s found most sufferers to be anxious, tense, and perfectionistic. [70]
There was, however, no control group for the subjects. Current consensus
does
not support a psychosomatic origin for either proctalgia fugax or levator
ani
syndrome, [91] although stressful events may trigger attacks. [23] [73]
Diagnosis and Clinical Features
Grant et al [27] in an analysis of 316 cases observed that patients with
levator ani syndrome complained of a vague, indefinite rectal discomfort or
pain. The pain was felt high in the rectum and was sometimes associated with
a
sensation of pressure like a ball or other intrarectal object. Others note
the
pain may be aggravated by sitting or by the need to defecate, and relieved
by
walking or lying down. [18] [23]
By definition, the pain of proctalgia fugax is brief and self limited.
Patients with proctalgia fugax complain of sudden onset of intense, sharp,
stabbing or cramping pain in the anorectum. The pain occurs at any time of
the
day and typically awakens the sufferer from a sound sleep. [14] [27] [29]
[67]
[73]
The physical examination of patients with levator ani syndrome and
proctalgia
fugax usually is unremarkable. [4] [60] [91] In patients with levator ani
syndrome, palpation of the levator muscle while performing a digital rectal
examination usually reproduces their pain. Grant noted that in patients with
levator ani syndrome, their levator muscle may be felt as a firm band
beneath
the examining finger as it is passed from a lateral to an anterior
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60
position within the rectum. He also observed these patients had tenderness
of
the levator muscle, and that in most it was unilateral and on the left, a
finding confirmed by others. [27] [34]
There are no diagnostic studies to exclude or confirm levator ani syndrome
or
proctalgia fugax. The inexperienced practitioner should consider other
causes
of anorectal pain and obtain further investigations or consultations as
appropriate. [34] [59] [66] [80] Other causes of anorectal pain are *
Anal fissure
Endometriosis
External hemorrhoids (thrombosed or infected)
Fecal impaction or foreign body
Myopathy (hereditary)
Neoplasm (anorectal, ovarian, or prostatic)
Perirectal abscess
Prostatitis
Treatment and Patient Education
Management of levator ani syndrome and proctalgia fugax is controversial. No
single treatment has been unusually successful in all patients. Patients
with
levator ani syndrome and proctalgia fugax should be reassured that their
painful attacks are benign and often diminish over time.
Levator Ani Syndrome
For patients with levator ani syndrome, initial conservative treatment with
hot baths, nonsteroidal anti-inflammatory drugs, muscle relaxants, or
levator
muscle massage is recommended. [18] [27] [66] Levator muscle massage
consists
of high, deep, digital pressure over the puborectalis portion of the levator
floor. [18] This procedure is repeated every 2 to 3 weeks for two to three
courses. [27] One-half to two-thirds of levator ani syndrome sufferers
improve
with the above measures. [18] [27]
In the 1980s, several researchers tried electrogalvanic stimulation of the
levator muscle. Early studies reported a 90% success rate, [59] [80] but
subsequent investigations demonstrated a long-term failure rate of 32% to
60%.
[6] [34] [66] More recently, researchers using EMG-based biofeedback have
shown improvement in pain in some studies. [23] [33] The findings of these
studies may be unreliable because of the small number of subjects, lack of
controls, and high dropout rate.
Proctalgia Fugax
Recommendations for treatment of proctalgia fugax are limited to anecdotal
reports and a single randomized controlled trial. Fortunately for most
patients, the attacks are brief and infrequent. For patients with frequent
attacks, physical modalities such as hot packs or direct anal pressure
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* Data fromReferences [18] [60]
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61
with a finger or closed fist may alleviate the pain. Diltiazem has helped at
least two patients, and oral clonidine provided relief for another. [7] [29]
[82] A recent, randomized, controlled trial of albuterol in 18 patients with
proctalgia fugax showed significant reduction in duration of pain compared
with placebo. [13] Although intriguing, the authors could not commit to
recommending albuterol for proctalgia fugax without further studies
confirming
efficacy.
PRURITIS ANI
Definition and Epidemiology
Pruritis ani is an unpleasant cutaneous sensation that induces that desire
to
scratch the skin around the anal orifice. [32] [81] The exact incidence
worldwide is unknown; it reportedly occurs in as many as 45% and as few as
1%
of the population. [2] [32] It occurs more often in men, with the observed
male-to-female ratio varying from 2:1 to 4:1. [11] [44] [81] Most patients
are
30 to 70 years old. [79] [87] Pruritis ani can be classified as primary
(idiopathic) or secondary.
Causes of secondary pruritis ani are *
Anorectal disorders
Benign
Fissures
Hemorrhoids
Proctitis (idiopathic and ulcerative)
Abscess
Fistula
Neoplastic
Rectal cancer
Adenomatous polyp
Colon cancer
Dermatologic disorders
Benign
Lichen planus
Lichen sclerosis et atrophicus
Psoriasis
Seborrhea
Neoplastic
Squamous-cell carcinoma
Bowen's disease
Extramammary Paget's disease
Infectious disorders
Fungal
Candida albicans
Dermatophytes
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* Data fromReference [2] [11] [26] [32] [89] [90]
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62
Bacterial
Staphylococcus aureus
Corynebacterium minutissimum (erythrasma)
Group A beta-hemolytic streptococci
Viral
Human papillomavirus (condyloma acuminata)
Herpes simplex
Parasitic
Enterobius vermicularis (pinworms)
Sarcoptes scabiei
Medications
Systemic
Antibiotics
Colchicine
Quinidine
Mineral oil
Topical
Local anesthetics (caine derivatives)
Neomycin
Witch hazel
Systemic diseases
Diabetes mellitus
Lymphoma
Causes of idiopathic (primary) pruritis ani are *
Diet
Foods
Tomatoes
Citrus fruits
Nuts
Chocolate
Dairy products (milk, cheese, ice cream)
Spices (Mexican, Italian, barbecue)
Beverages
Coffee
Tea
Cola
Beer
Miscellaneous irritants
Fecal soiling
Excessive moisture
Soap
Aggressive anal wiping
Scented toilet paper
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* Data fromReference [2] [11] [20] [26] [32]
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63
Cause and Pathophysiology
Pruritis ani is a symptom complex, not a diagnosis. It is estimated that 25%
to 75% of patients with pruritis ani have an associated disorder. [2] [8]
[11]
[26] [32] [89] [90] These patients with so-called secondary pruritis ani
usually respond to treatment of the underlying condition. It has been
suggested that psychological factors may play a role in the genesis of anal
itching. [87] Research, however, does not support this perception. [44] [79]
Approximately one-half of patients with perianal pruritis have no
identifiable
anal or rectal disease. These patients can be difficult to treat, but
frequently improve following modification of diet and perianal hygiene
habits.
In 1977 Friend [20] proposed that patients with idiopathic pruritis ani
consume enormous quantities of liquids and that certain beverages--coffee,
tea, cola, and beer--were especially likely to produce anal itching. He
suggested that there is a threshold above which patients develop pruritis
ani
from certain food items and below which they do not. [20] Furthermore, he
observed a 24- to 48-hour delay in the onset of symptoms after the threshold
was exceeded. Although most authorities agree that patients with pruritis
ani
should avoid coffee (including decaffeinated), alcohol, and caffeinated
drinks, Friend's hypothesis has never been studied in a randomized
controlled
trial. [11] [26] [32] [81]
The pathophysiology of all the secondary causes of pruritis ani is beyond
the
scope of this article. Little is known about the pathogenesis of idiopathic
pruritis ani. Smith et al hypothesized that fecal leakage caused skin
irritation and subsequent pruritis. They proposed a mechanism whereby
several
factors including stress, diet, and anatomic anal changes produced
accidental
fecal soiling. Indeed, anal manometric studies of patients with pruritis ani
demonstrate an increase in anal sphincter relaxation and subsequent fluid
leak
following rectal distension. [1] [16]
Although no difference in fecal microflora in patients with pruritis ani has
been found, it is thought that bacterial endopeptidases, exotoxins, and
intestinal lysozymes may act as irritating agents. [26] [78] If the sufferer
scratches and breaks the sensitive perianal skin, these substances might
penetrate into the dermis causing inflammation and release of other
irritating
compounds. [26] Therefore, more itching and scratching ensue, creating a
vicious cycle. Many patients add insult to injury by attempting to clean the
area with harsh soaps and vigorous rubbing, or by applying topical
medications
that further irritate the skin. Other factors such as increased perianal
moisture from sweat also may contribute to the problem.
Diagnosis and Clinical Features
Patients with pruritis ani usually report an escalating pattern of itching
and
scratching in the perianal region. These symptoms may be worse at night when
they are less distracted by usual daily activities. The clinician
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64
should ask the patient about anal hygiene and dietary habits, fecal soiling,
and associated medical conditions.
Examination of the perianal area may reveal maceration, erythema,
excoriation,
and lichenification. The practitioner should perform a digital rectal
examination and anoscopy to assess the sphincter tone and look for secondary
causes of pruritis suggested from the history. Initially, an exhaustive
search
for associated or causative conditions usually is not necessary. At least
one
study recommends an aggressive work-up of patients over age 50 or who have
had
symptoms for several weeks. [11] Patients who fail to respond to 3 or 4
weeks
of conservative treatment should undergo further investigations such as skin
biopsy and sigmoidoscopy or colonoscopy. [58]
Treatment and Patient Education
The management of pruritis ani is directed towards the underlying cause.
Most
patients with secondary pruritis ani improve following treatment of the
primary disorder. [71] If the diagnosis is idiopathic, then the patient is
taught principles of good anal hygiene and instructed to modify his or her
diet. Several patient self-care instructions have been published. [2] [20]
[32] [79] [81] In general, pruritis ani sufferers are advised to clean the
perianal area with water following defecation, but to avoid using soaps and
vigorous rubbing. Following this, the patient should dry the anus with a
hair
dryer or by patting gently with cotton. Between bowel movements he or she
should place a thin cotton pledget dusted with unscented cornstarch against
the anus. A high fiber diet is recommended to regulate bowel movements and
absorb excess liquid. Finally, the patient should eliminate all foods and
beverages that may be exacerbating the itching. Once the symptoms have
resolved, the patient can cautiously add these dietary items one at a time,
keeping a food and symptom diary to see if there is a threshold phenomenon.
[20]
Topical medications generally are not recommended because they may cause
further irritation. If used, a bland cream such as zinc oxide or mild
corticosteroid such as 1% hydrocortisone cream should be applied sparingly
two
to three times a day. [2] [26] [32] [81] More potent fluorinated
corticosteroids should be avoided as they may worsen the problem by causing
skin atrophy. [32] [87] Agents such as aluminum acetate, crotamiton, and
magnesium hydroxide in phenol are no better than bland creams in the
treatment
of pruritis ani. [2]
Systemic therapy with an antihistamine such as diphenhydramine (Benadryl) or
hydroxyzine (Atarax, Vistaril) may relieve the itching and allow the patient
to sleep. [26] Recalcitrant cases of pruritis ani are uncommon, and
clinicians
treating these patients should search for a secondary cause of the itching.
It
is advisable to refer patients with intractable idiopathic pruritis ani to a
dermatologist, gastroenterologist, or colorectal surgeon for treatment.
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65
CONCLUSION
Anal fissures, proctalgia fugax, levator ani syndrome, and pruritis ani are
common afflictions. The clinician who obtains a thorough history and
performs
a complete examination can accurately diagnose these disorders. Ancillary
tests are seldom helpful and rarely necessary. Most patients suffering from
these conditions readily respond to conservative therapy provided in the
primary care practitioner's office. Most patients with anal fissures improve
with stool softeners, sitz baths, and application of a mild corticosteroid
cream; however, some patients require an operation. New, nonsurgical methods
are being developed that may reduce the need for surgical intervention.
Patients with perirectal pain should be examined thoroughly for potentially
curable causes of their discomfort. If levator ani syndrome or proctalgia
fugax are confirmed, the patient should be reassured concerning the benign
nature of the attacks. The ideal remedy for levator ani syndrome is not
known,
but some patients may obtain relief from nonsteroidal anti-inflammatory
drugs,
muscle relaxants, levator muscle massage, electrogalvanic stimulation, or
biofeedback. Proctalgia fugax rarely requires specific treatment since
attacks
are brief and self-limited. Patients with pruritis ani should be taught
principles of good anal hygiene, told to reduce their fluid intake, and
avoid
anorectal trauma such as rubbing or scratching.
ACKNOWLEDGMENT
The author acknowledges the Swedish Medical Center Library Staff for their
help in obtaining material for this article.
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This communication is intended to provide general information, and in
no way is a substitute for face-to-face medical care. No implication
of a doctor-patient relationship should be assumed by the reader.
Best regards,
Jordan Dimitrakov, MD, PhD
Are you a twin with CPPS or IC? Do you have a brother, sister, or other
relatives with CPPS/IC? If you want to make a change, help yourself and
others with these devastating conditions, please e-mail me at:
jdimi...@my-deja.com. Anonymity guaranteed!
bud
>
> In accordance with Murphy's Law, it seems I have now developed a case of
> hemorrhoids on top of my prostatitis
Are you taking saw palmetto by any chance? My butt problems went away
as soon as I stopped taking saw p. It did not agree with my insides,
and it took me a long time to figure it out.
Thad Noles
(for those that are sensitive to it) is diarrhea, which can definitely give
you hemorrhoids if you have it bad enough. (Lovely conversation topic, eh?)
Anyway, this is what gave it to me. In my overzealous, panicked race to
obtain some relief, I began taking flax oil AND eating flax cereal to get
the EFAs (anti-inflammatory). A LOT of cereal. I don't recommend eating a
lot of bran-containing cereal unless you give yourself some time to adjust
to it. The consequence could be unpleasant :). I have since backed off on
the cereal.
As a side note, however, the flax oil has reduced the inflammation in my
prostate since it flared up.
bud wrote in message <3AAA5F...@bud.com>...