Abdo

minal
Abdominal Pain: Etiological Classification
Pain Originating in the Abdomen:
Bacterial contamination:
Perforated appendix or other perforated viscus
Pelvic Inflammatory disease
Vascular disturbances:
Embolism or thrombus
Vascular rupture
Pressure or torsional occlusion
Sickle cell Anaemia
Chemical Irritation:
Perforated ulcer
Pancreatitis
Mittelschmerz Abdominal wall:
Distortion or traction of the mesentery
Trauma or infection of the muscles
Mechanical Obstruction of Hollow Viscera:
Obstruction of the small or large intestine
Obstruction of the biliary tree
Obstruction of the ureter Vascular disturbances:
Distention of the viscer
al surfaces
Example: by Haemorrhage: Hepatic/Renal capsules
Inflammation of a viscus:
Appendicitis
Typhoid fever
Typhilitis
Pain referred from an extra-abdominal source:
Cardiothoracic:
Acute Myocardial Infarction
Myocarditis, Endocarditis, Pericarditis
Congestive cardiac failure
Pneumonia
Pulmonary embolus
Pleurodynia
Pneumothorax
Empyema
Oesophageal disease, spasm, rupture, inflammation
Genatilia:
Torsion of the testis
Metabolic causes:
Diabetes
Uraemia
Hyperlipidemia
Hyperthyroidism Acute adrenal insufficiency
Familial Mediterranean Fever
Porphyria
C1 esterase inhibitor deficiency (angioneurotic oedema)
Neurological/Psychiatric Causes:
Herpes zoster
Tabes dorsalis
Causalgia
Radiculitis from infection or arthritis Spinal cord or nerve root compression
Functional disorders
Psychiatric disorders
Toxic causes
Lead poisoning

Insect or Animal envenomations: Black widow spiders, Snake bites

Uncertain mechanisms:
Narcotic withdrawal
Heat stroke
The pain intensity is determined by the type and quantity of the inciting agent,
in a given duration of time.
A small quantity of gastric acid (sterile) released into the peritoneal cavity c
auses much more pain compared to the release of the same amount of grossly conta
minated neutral faecal matter. Pancreatic juice incites more pain, containing en
zymatically active material.
Blood and urine on the other hand go unnoticed if their contact with the periton
eum hasn't been sudden or massive.
Bacterial contamination causes pain, which is frequently of low intensity early
in the illness (such as pelvic inflammatory disease) until the bacterial multipl
ication leads to elaboration of irritating substances.
Pain of peritonitis is invariably emphasized by pressure or changes in the tensi
on of the peritoneum, whether produced by movement or by palpation.
Patient suffering with peritonitis usually lies quiet in his/her bed, a complete
contrast to a patient with colic who is seen writhing with pain.
Tonic reflex spasm of the musculature of the abdomen is another characteristic f
eature of peritonitis. The location of the involved body segment, the rate of de
velopment of the inflammatory process and the integrity of the nervous system de
termines the intensity of the tonic muscle spasm.
Obstruction of hollow viscera:
Pain in this scenario is colicky.
may not be present in all the cases.
The colicky pain of obstruction of the small intestine is usually peri-umbilical
or supra umbilical, and poorly localized.
The colicky nature of the pain may subside after a while when the tone of the mu
scle is lost due to progressive distention of the intestine.
Pain may spread to the lower lumbar region due to traction on the root of mesent
ery when strangulation superimposes obstruction.
The colicky pain of the colonic obstruction is of lesser intensity and usually f
elt in the infra-umbilical area.
Lumbar radiation of pain is common in colonic obstruction.
Biliary colic is a misnomer, since the pain usually results from a sudden disten
tion of the biliary tree.
Distention of the gall bladder (acute) causes pain in the right upper quadrant w
ith radiation to the right posterior region of the thorax or to the tip of the r
ight scapula, sometimes to the midline.
Distention of the common bile duct is usually associated with pain in the epigas
trium radiating to the upper part of the lumbar region.
The pain due to distention of the pancreatic ducts is similar to the pain of the
distention of the common bile duct with an added feature of being accentuated b
y recumbency and relieved by the upright position.
Urinary bladder obstruction causes a dull, supra-pubic pain, which is low in int
ensity.
Ureteric obstruction is characterized by a severe supra-pubic and flank pain, wh
ich radiates to the penis, scrotum or the inner aspect of the thigh.
Obstruction in the pelvi-ureteric junction is felt as pain in the costovertebral
angle.
Vascular abnormalities:
Pain associated with vascular disturbances isn't always sudden or abrupt in onse
t. The pain of an embolism or thrombosis of superior mesenteric artery or that o

f an impending rupture of the abdominal aortic aneurysm is certainly severe and

abrupt in onset. But it is noteworthy that patients with a superior mesenteric a
rtery occlusion may have mild continuous or cramping diffuse pain two or three d
ays prior to the vascular collapse or before the onset of findings pertaining to
peritonitis. This early discomfort is usually a result of hyperperistalisis and
not the irritation of the peritoneum. Thus it is likely that the presence of co
ntinuous, diffuse pain in the absence of peritoneal signs (such as tenderness or
rigidity) is likely to be a result of vascular disturbances, being quite charac
teristic of the superior mesenteric artery occlusion. A radiating abdominal pain
(to the scrotum, perineum, etc.) is usually due to rupturing abdominal aortic a
neurysm. The pain may begin and persist for several days prior to the actual rup
ture and subsequent circulatory collapse.
Pain arising in the Abdominal Wall:
Pain arising from the abdominal wall is usually constant and aching. Prolonged s
tanding, movement and pressure increase the discomfort and the muscle spasm. Hae
matoma in the rectus sheath usually presents as a mass in the lower quadrants of
the abdomen. If only the muscles of the abdominal wall is involved, it usually
is due to a local pathogenesis as opposed to the possible diagnosis of myositis
of the muscles of the abdominal wall which is likely if other muscle groups in t
he body are also involved.
Referred Pain:
An important dictum is that the possibility of intra thoracic disease must be co
nsidered in every patient with abdominal pain, especially if the pain is in the
upper part of the abdomen.
Diaphragmatic pleuritis as a result of pneumonia or pulmonary infarction may cau
se pain in the right upper quadrant and pain in the supra clavicular area.
Referred pain of thoracic origin is usually accompanied by splinting of the invo
lved hemithorax with respiratory lag and decrease in excursion more marked than
thatseen in the presence of intra-abdominal disease.
The apparent abdominal muscle spasm will decrease during inspiration when it is
due to a thoracic cause, but persists during both phases of respiration when the
pain is abdominal in origin.
When the area where the referred pain is perceived is palpated, there is usually
no increase in the intensity of pain.
Metabolic Abdominal Crises:
C1 esterase deficiency causing Angioneurotic oedema is frequently associated wit
h episodes of severe abdominal pain.
The pain of porphyria and of lead colic is usually difficult to distinguish from
that of intestinal obstruction but severe hyperperistalisis is a feature of bot
h.
The pain of uraemia or diabetes is non-specific and the site and type of pain fr
equently shift.
Diabetic acidosis may be precipitated by appendicitis or intestinal obstruction.
If there isn't a prompt resolution of the pain after the correction of the meta
bolic abnormalities, an underlying organic problem may be suspected.
Neurogenic Causes:
In diseases where there is injury to sensory nerve fibres, causalgic pain may en
sue (see chapter on Complex regional pain syndrome- CRPS).
Normal stimuli such as touch or change in temperature may be transformed to this
type of pain.
This is frequently seen in a patient at rest.
Even though the pain may be triggered by gentle touch, there is no abdominal rig

idity that is so common with intra-abdominal disease.

Pain is independent of food consumption and there is usually no disturbance of r
espiration or any distention of the abdomen.
Pain may also result due to herpes zoster or impingement of the nerve by arthrit
is, tumours, herniated nucleus pulposus, diabetes or syphilis, wherein the pain
arises from the spinal nerve roots and comes and goes suddenly and is of the lan
cinating type.
Tabes dosralis may cause severe muscle spasm (gastric crisis).
Pain due to functional causes doesn't conform to any of the above-mentioned patt
erns of pain.
The pain here is hard to define and the diagnosis is made by fulfilling the defi
ned diagnostic criteria, which is exclusive to the particular underlying cause.
Example of a one such condition that causes functional abdominal pain includes I
rritable bowel syndrome (IBS).
A differential diagnosis may also be established based on the location of the pa
in, as we have seen above and detailed in the diagram below:
Sometimes, as explained above, the pain may be diffuse and it may not be possibl
e to localize it. Such pain may be due to:
Gastroenteritis
Mesenteric ischaemia
Bowel obstruction
Irritable bowel Syndrome
Peritonitis
Diabetes
Malaria
Familial Mediterranean fever
Metabolic disorders
Psychiatric disorders.

Acute pancreatitis:
Acute pancreatitis is an inflammatory process causing a premature release of act
ivated pancreatic enzymes precipitating auto digestion and pain.
It is one of the most common causes of abdominal pain. Acute pancreatitis has ma
ny causes:
Common causes of Acute Pancreatitis
Alcohol abuse
Gall stones
Viral infections
Medications
Metabolic causes
Connective tissue disorders
Tumour obstruction of the ampulla of Vater
Heriditary
Nausea, vomiting, and anorexia are other common features.
Signs and Symptoms:
Patient appears ill and anxious
Tachycardia and hypotension (from hypovolemia)
Low grade fever

In a few patients: pulmonary complications such as pleuritic pain and pleural ef

fusion
Diffuse abdominal tenderness with peritoneal signs
Pseudocyst may form and may be palpable
If haemorrhage occurs:
o
Periumbilical ecchymosis = Cullen's sign
o
Flank ecchymosis = Turner's sign
Hypocalcemia may occur presenting with Trosseau's sign or Chvostek's sign.
Investigations:
The standard laboratory test is the measuring and monitoring the levels of serum
amylase, which tend to peak at 48 to 72 hours and then begin to normalize.
Serum lipase levels remain elevated and are better correlated with the severity
of the disease.
Plain radiographs of the chest are important
Other laboratory tests, in view of the extra-pancreatic effects include: complet
e blood picture with a differential count, serum calcium, serum glucose, liver f
unction tests and electrolytes
CT scan of the abdomen helps identify a pancreatic pseudocyst.
Gall bladder evaluation is indicated if gallstones are considered a cause
Arterial blood gas analysis helps evalutate and look for metabolic acidosis and
respiratory failure.
Differential Diagnosis
Perforated peptic ulcer
Acute cholecystitis
Bowel obstruction
Renal calculi
Mesenteric infarction
Myocardial infarction
Diabetic ketoacidosis
Pneumonia
Treatment:
Most cases are self-limiting and resolve within a period of 5 to 7 days.
The initial treatment is always allowing the pancreas to rest. This is achieved
by keeping the patient nil by mouth NBM), thereby decreasing the serum gastrin s
ecretion and, if ileus is present, by instituting nasogastric suction.
Short acting opioid analgesics would be next in order to control the level of pa
in. Meperidine is a good alternative if ileus is present. Opioid analgesics have
a notorious effect of suppressing the cough reflex and respiration, and hence t
he patient requires monitoring and adequate pulmonary toilet techniques.
CT scan guided celiac plexus block is indicated if the pain continues at a high
intensity despite analgesics. The block is instituted with a local anaesthetic.
A continuous thoracic epidural block with a local anaesthetic or opioid or bith
may be adequate to achieve pain control, while avoiding respiratory depression i
n the patient.
Hypovolemia should be treated aggressively and immediately with colloid and crys
talloid infusions.
Surgical drainage and removal of necrotic tissue may be necessary and important
in severe necrotizing pancreatitis.
Pain of Chronic pancreatitis:
Chronic pancreatitis refers to inflammation causing permanent structural damage
to the pancreas.
CAUSES:
Alcoholism
Trauma Cystic Fibrosis Infection
Coxsackie B virus
Cytomegalovirus
Mumps
Mechanical
Gall stones
Pancreatic intraductual stones/plugs
Pancreas divisum

Pancreatic cancer
Periampullary cancer
Sphincter of Oddi stenosis
Endoscopic Retrograde Cholangiopancreatography (ERCP)

induced Metabolic Distru

bances
Hypertriglyceridemia
Hypercalcemia
Hyperparathyroidism
Autoimmune Disease
SLE
Sjogren's syndrome
Primary sclerosing cholangitis Medications
ACE inhibitors
Asparaginase
Azathioprine
Furosemide
Sulfa drugs
Valproate
Males are usually more frequently
Pancreatitis as a whole is classified as
Acute pancreatitis
Chronic calcifying pancreatitis
Chronc obstructive pancreatitis
Chronic inflammatory pancreatitis
TIGAR-O is a risk factor classification
*SAPE = Sentinel Acute Pancreatitis Event
The above illustration also helps show the various theories involved in the path
ogenesis of chronic pancreatitis. A brief look at the individual theories:
Oxidative stress theory:
An over-activity of the hepatic mixed-function oxidases precipitates pancreatic
disease. Secretion of oxidized compounds into the bile leads to the contaminatio
n of the pancreatic ducts, which leads to oxidative damage to the acinar and duc
tal cells. Inflammation and fibrosis occurs if this damage is repeated and prolo
nged.
Toxic-metabolic theory:
The direct toxic effects of alcohol impair the intra-cellular metabolism of the
acinar cell. Fatty degeneration, cellular necrosis and fibrosis are a result of
cytoplasmic lipid accumulation within the acinar cells. Fatty acid esters, which
result from alcohol metabolism, are the toxic substances, rather than alcohol i
tself. It must be remembered that not all chronic alcoholics develop pancreatiti
s. Thus alcohol acts as an environmental factor, which combines with the genetic
factors to cause damage.
Other toxins and metabolic conditions are associated with the development of chr
onic pancreatitis. Smoking is an independent risk factor, distinct from alcohol
intake. Smokers with chronic pancreatitis also have higher pain-scores compared
to non-smokers.
Hypercalcemia and renal failure are important causes of pancreatitis through the
toxic-metabolic mechanisms.
The stone and duct obstruction theory:
In acute pancreatitis, tissue damage is secondary to uncontrolled activation of
trypsin, which leads to auto-digestion of the pancreatic tissue. The pattern and
process leading to tissue damage is different in chronic pancreatitis. In chron
ic pancreatitis, alcohol alters the exocrine function in the pancreas leading to
increased formation of stones and protein plugs. Over time, these stones within

the pancreatic ducts lead to scarring, obstruction, stasis, atrophy and fibrosi
s.
Necrosis-Fibrosis theory:
This requires the existence of previous recurrent attacks of acute pancreatitis.
Repeated pancreatitis attacks causes inflammatory changes with necrosis, which
leads to scarring in the peri-ductular areas. The ductules become obstructed and
stasis of the pancreatic fluid leads to stone formation, which causes obstructi
on and thus is followed by atrophy and fibrosis.
The development of chronic pancreatitis depends upon the frequency and severity
of attacks of acute pancreatitis.
Sentinel Acute pancreatitis event hypothesis:
the first episode of acute pancreatits was emphasized
result of unregulated trypsinogen activation
produces a massive inflammatory respose that occurs over early and late phases.
Pathogenesis of pain in chronic pancreatitis:
To understand it simple, chronic pancreatitis could be divided into large duct o
r small duct disease. The former is the result of obstruction from stones or fib
rosis.
pain of the chronic pancreatitis regard neuronal damage leading to the periphera
l sensitization and the resultant central sensitization
The central nervous system is altered by prolonged and repeated attacks of pain
in chronic pancreatitis. Using EEG, changes have been noted in the limbic system
and in the cortical centres such as the anterior cingulate gyrus.
Chronic pancreatitis leads to changes in the cortical projections of the nocicep
tive system. This is evident with the fact that total pancreatectomy in patients
with chronic pancreatitis fails to relieve pain in ~30%.
It has been hypothesized that along with the anatomical and neuronal mechanisms,
the immune system is involved. The immune system has a 'salutogenic' mechanism,
perpetuating the cycles of inflammation and ongoing pain, the salutogenic respo
nse being the modulation of the immune response by the centres in the brain.
Treatment Strategies:
Life style changes:
Alcohol:
Alcohol abstinence is an important and necessary step when there is a history of
alcohol abuse. This is found useful even in those patients where there are othe
r established causes for the panceratitis.
Smoking:
All patients suffering from pancreatitis should be encouraged to quit smoking si
nce (as explained earlier); smoking is an independent risk factor for chronic pa
ncreatitis. It accelerates the progression of the disease and worsens the percep
tion of pain.
Diet:
tochopherol, riboflavin, magnesium, choline, copper, manganese and sulphur.
low-fat diet, and given vitamin supplements and anti-oxidant therapies.
Pharmacological therapy:
Analgesics:
combination of paracetomol and an opioid drug. Tramadol is given commonly at a d
ose of 50 to 100 mg four times a day.
Parenteral opioid (IV Morphine) is usually started in patients brought to an eme
rgency unit with severe pain due to chronic pancreatitis. Early conversion there
after from IV to oral medications is recommended when opioids are administered.

Examples of drugs used to treat the pain of chronic pancreatitis:

Drug class
Examples
Simple Analgesics
Paracetomol
Aspirin
Other NSAIDs
Weak opioids
Codeine
Tramadol
Buprenorphine
Strong opioids
Morphine
Fentanyl
Pethidine
Oxycodone
Methadone
Hydromorphone
Anti-depressants
Amitriptyline
Nortriptyline
Fluoxetine
Paroxetine
Gabapentinoids
Gabapentin
Pregabalin
NMDS (N-methyl-d-aspartate) receptor antagonists
Ketamine
S-Ketamine
It is important to determine if the pain in acute-on-chronic, secondary to infla
mmation in the panbcreas or a flare-up of pain that is seen in the natural progr
ession of chronic pancreatitis.
The former is usually short-lived with episodes lasting less than 10 days, separ
ated by a long pain-free interval which itself could last for several months, wh
ile the latter is characterized by prolonged periods of consistent pain which ma
y last for months, being exacerbated by severe, worsening pain superimposed on e
xisting background pain.
Unless there are complications, the latter group of patients doesn't require a p
rolonged hospital stay, and a readjustment of the dose of analgesics is required
.
Non-pharmacological therapy:
Nerual Interruption: This includes blocking the neuronal transmission of pain in
chronic pancreatitis either by bilateral thoracoscopic splanchinectomy (BITS) o
r by a celiac plexus block.
Endoscopic therapies in chronic pancreatitis:
Endoscopic retrograde cholangiopancreatography
Surgical treatment for the pain of Pancreatitis:

Chronic Prostatitis
Chronic prostatic pain in an individual may present as a recurrent or persistent
pain in the region of the prostate, associated with symptoms, usually suggestiv
e of urinary tract and/or sexual dysfunction, and in most cases there is no evid
ence of an infection or associated pathologies.
Chronic prostatitis/chronic pelvic pain syndrome is a common but poorly understo
od condition. This condition was previously referred to as 'non-bacterial' prost

atitis.
Chronic prostate pain syndrome is defined as "a pain in a man's pelvic region th
at persists for at least 3 months, often accompanied by voiding difficulties and
effects on sexual function (usually pain related to ejaculation)"
Symptoms tend to be episodic, relapsing and intermittent.
Though the name indicates and inflammatory pathogenesis, this condition is by no
means associated with an inflammation of the prostate gland, and we can go even
further to say that it is not, by any proven state, a disease of the prostate.
Symptoms of Chronic prostate pain syndrome:
Persistent urinary urgency
Dysuria
Poor urinary flow
Perineal discomfort
Pain
Radiating pain to the low back, suprapubic area and groin
Pain on ejaculation
The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDKD) of
the National Institutes of Health (NIH) classify prostatitis as:
Classification (category)
Entity included
NIH I Acute bacterial prostatitis
NIH II Chronic bacterial prostatitis
NIH III
IIIA
IIIB
Chronic
Inflammatory
Non-inflammatory
NIH IV Asymptomatic inflammatory
The above classification however is schemed with the assumption that an infectio
n is the causative event. Mid-stream urine is collected for culture, and those w
ith the culture positive for uropathogens are classified under
NIH I or acute bacterial prostatitis, while those with chronic symptoms and a po
sitive urine culture are diagnosed with NIH II.
NIH III is defined by a negative mid-stream urine culture and this entity is wha
t is now referred to as "chronic prostatitis" or "chronic prostate pain syndrome
". This is sub categorized into NIH IIIa and NIH IIIb. This categorization is ba
sed on the presence (IIIa) or absence (IIIb) of leukocytes in the prostatic flui
d expressed by prostatic massage.
While examining a patient and chronic prostatitis is suspected, it bodes well to
remember that the physical examination in most cases is typically normal. There
would be no tenderness on palpation, essentially pointing away from an inflamma
tory process.
Urodynamic studies are done which usually reveal:
Decreased urinary flow rates
Incomplete relaxation of the bladder neck and the prostatic urethra
Abnormally high urethral closure pressure at rest.
The enumeration of leukocytes in the prostatic fluid by bright field microscopy
distinguished the type IIIa from IIIb, the former being inflammatory and the lat
ter being non-inflammatory
Treatment:
The exact cause of the prostate pain of this syndrome is not exactly known. Most
patients require a multi-modal approach for pain relief and keeping the pain at
bay.
Alpha blockers: such as terazosin, alfuzosin, doxazosin, tamsulosin, reduce the
urinary symptoms and pain. An alpha blocker is required to be given for 3 to 6 m
onths before reassessing or rethinking the treatment options for lack of a posit
ive response to the said group of drugs.
Widely, an empirical antibiotic therapy is used since improvement has been seen
in many patients on antimicrobial drugs. Patients responding to antibiotics must
be maintained on the medication for 4 to 6 weeks or longer. Antibiotics commonl
y used include Ciprofloxacin, Ofloxacin, etc. A call on the antibiotic may be ta

ken depending on the pathogen found on urine culture and its sensitivity report.
Non-steroidal anti-inflammatory drugs may be useful for pain relief in some pati
ents.
Cytokine inhibitors may be useful, acting as immune-modulators. Corticosteroids
are generally not effective.
Opioids bring about a moderate pain relief in patients with refractory prostate
pain syndrome.
5-a reductase inhibitors such as finasteride may improve voiding and pain.
Muscle relaxants are believed to be helpful in sphincter dysfunction or pelvic f
loor/perineal muscle spasm.
Supportive treatment modalities include biofeedback, relaxation exercises, lifes
tyle modification, acupuncture, massage therapy, etc. has all received claim and
recommendations to improve symptoms.
Surgical intervention includes transurethral incision of the bladder neck, radic
al transurethral resection of the prostate or radical prostatectomy. These techn
iques have a very limited role to play and require an additional and specific in
dication.

Testicular Pain
Testicular pain or Orchialgia or Orchidynia refers to recurrent or persistent pa
in that is localized to the testis, with the patient presenting with symptoms su
ggestive of a urinary tract infection or sexual dysfunction.
Orchialgia can be divided based on multiple factors:
Basis of classification of Orchialgia Types of Orchialgia
Time/ Duration of pain Acute or Chronic
Age at onset
Paediatric or Adult
Anatomic site Referred pain or Non-referred pain
Pathology
Mechanical or Infectious
Severity
Mild or Severe
Treatment
Conservative/Supportive or Surgical
Other causes: Medication Induced or Physical or Psychiatric
Reality Real pain or Malingering
Pathophysiology:
Nerve supply to the testis:
The autonomic supply to the testes and the epididymis is mostly sympathetic and
originates from T10-L1 segment. About 10% of the autonomic nerve supply is paras
ympathetic.
The spermatic plexus is a group of autonomic fibres that follows the internal sp
ermatic vessels, the testicular artery and vein and the vas deferens to the epid
idymis and the testis.
Three nerve groups contribute to the spermatic plexus:
The superior spermatic nerves
The middle spermatic nerves
The inferior spermatic nerves.
superior spermatic nerves, composed of fibres from
intermesenteric and the renal plexuses
This association between the intestinal nerves and the nerves of the testes
may account for the visceral manifestation of testicular trauma, referred to as
'sick stomach' by the patients.
The middle spermatic nerves arise from the fibres of the superior hypogastric pl
exus.
The inferior spermatic nerves arise from the pelvic plexus or the inferior hypog

astric plexus and may provide significant sympathetic output top the testis.
The somatic supply to the testes and the scrotum originates from L1 and L2 nerve
roots through the iliohypogastric, ilioinguinal and genitofemoral nerves.
Damage to the nerve supply of the testis or directly to the testis or the epidid
ymis results in orchialgia. Lesions affecting the somatic structures in the same
segmental nerve supply as the testes (L1 and L2) may refer pain to this area.
Pain is usually sympathetically maintained, when it is caused by damage to the a
forementioned structures. Thus patients who don't find any significant pain reli
ef from inguinal denervation or subcutaneous blockade, find relief with pelvic p
lexus block.
Differential diagnosis:
Differential diagnosis
Referred pain:
Radiculitis
Nephrolithiasis
Ilioinguinal and genitofemoral neuralgia
Inguinal hernia
Tendinitis of the inguinal ligament
Abdominal aortic aneurysm
Appendicits
Epilepsy
Causative factors:
Testicular torsion
Torsion of the testicular appendage
Epididymitis, Scrotitis
Trauma
Surgery
Inguinal hernia
Tumour
Vasculitis
Henoch Scholein purpua
Idiopathic scrotal oedema
Blue balls (sexual frustration)
Hydrocoel
Varicocoel
Spermatocoel.
Diagnosis and treatment:
When orchialgia is suspected in a patient, a complete history and examination is
performed, with focus on the scrotal region.
History: focus of queries
Onset
Duration
Quality of pain
Relieving factors
Associated symptoms
Diurnal variation
Postural variation
Any sexual dysfunction
History of sexual abuse
Trauma
Past history:
Nephrolithiasis
Lumbar disk disease
Hernia
Prior inguinal surgery

It is not very common that the physical examination reveals an obvious cause of
pain. In most cases, the physical examination is normal. A detailed examination
is usually able to rule out causes of radicular pain. Palpation of the testis wi
ll help rule out other scrotal pathologies such as varcocoel ("bag of worms"), h
ydrocoel, etc. Patients may benefit from a semen analysis, especially and obviou
sly so when the present with complaints or signs of infertility.
Common laboratory tests:
Complete blood picture
Differential count
Urinalysis
Cultures
If there is pyuria or hematuria, the investigation proceeds in line as if there
was no pain to begin with, to find the underlying cause of the said pyuria or he
maturia.
If the results of the blood investigations and other lab investigations are norm
al, the next logical step would be to ask for a scrotal ultrasound. An overt abn
ormality would warrant a surgical consult.
Tumor markers should be asked for if a suspicion of a neoplasm exists (such as a
feto protein levels, human chorionic gonadotropin, lactate dehydrogenase, etc.).
Other investigational techniques include colour flow Doppler imaging, Radionucli
de scans, electromyography, MRI and needle aspiration.
Management:
Initial management:
Modification of postural and exertional habits would be the first step.
A scrotal suspension sling or a jock strap may provide symptomatic relief
Heat and cold therapy.
Trial of NSAIDs, oral antibiotics (even when cultures are normal; to treat Ureap
lasma or chlamydial infection).
The above is tried for a minimum of one month
Multi-disciplinary approach if the above fails:
Low dose antidepressant
NSAIDs
Long term opioid therapy
Antiepileptic drugs
TENS (Transcutaneous electrical nerve stimulation)
If this pain continues, then interventional therapy is initiated:
A spermatic cord block is given using a mixture of a local anaesthetic and corti
costeroid. The anaesthetic used is always epinephrine-free for this.
Similar blocks may be respectively given if the patients suffer from genitofemor
al or ilioinguinal neuralgia.
For patients not respnding to the spermatic cord block, local anaesthetic and th
e corticosteroid is applied to the pelvic plexus and this might provide relief.
Alternatively, the superior hypogastric plexus may be blocked.
Another approach is the lumbar sympathetic chain block at the T10
L1 level.
Surgical Management:
Surgical treatment may finally be necessary if all the conservative techniques h
ave failed to consistently provide a good degree of pain relief.
Orchidectomy is the usual last resort approach taken. A preferred approach is th
e inguinal route.
It is important to remember that the response to this procedure is not predictab
le. Pain may persist. An even bigger issue would be the profound effect on the m
ale psyche, thus other testicular sparing procedures are usually recommended and
preferred.
Spinal cord stimulation has been found to be effective in providing pain relief.
Select patients have the appropriate indications for this procedure.
Microscopic testicular denervation may produce and significant and near permanen
t pain relief. This technique, though requiring great skill and expertise, is ve
ry useful to the patients, being minimally invasive and entailing little morbidi
ty.
Chronic orchialgia is not a simple condition to deal with. It is important that

the treating physician is not oblivious to the great deal of emotional and psych
ological trauma that is caused by this condition. Despite the underlying cause f
or orchialgia being obscure, testicular cancer remains a very prominent possibil
ity and should always be kept in mind when forming a differential diagnosis and
investigating the patient.
Vulvodynia
Vulvodynia represents a syndrome of vulvar pain, sexual dysfunction and psycholo
gical distress. It is defined as a burning type (usually) of pain that
cannot be
consistently and tightly localized by
point pressure or instruments such as a cotton-tipped applicator.
The pain may occur with or without provocation by touch, pressure or friction.
Many attempts have been made to categorize varying types of vulvodynia. Some suc
h classifications include:
Primary vulvodynia
Secondary vulvodynia
Essential vulvodynia
Vulval vestibulitis
Cyclical vulvitis
Broad and brief anatomy:
The term vulva or pudendum refers to the external genitalia of the female gender
.
The following components make up the vulva:
Anterior to the vaginal and urethral openings is the mons pubis, which cushions
the symphysis pubis
From mons pubis arise two longitudinal folds of skin, the labia majora, exending
inferiorly and posteriorly. This is covered with pubic hair and has an abundanc
e of adipose tissue, sebaceous glands and apocrine sudoriferous glands. The labi
a majora are homologous to the male scrotum.
Medial to the labia majora are two smaller folds of skin called the labia minr,
which unlike the labia majora are devoid of pubic hair and adipose tissue and ha
ve few sudoriferous but many sebaceous glands. These are homologous to the spong
y (penile) urethra.
The clitoris is a cylindrical mass of two small erectile bodies, the corpora cav
ernosa and numerous nerves and blood vessels. The clitoris is homologous to the
male penis.
A layer of skin called the prepuce of the clitoris is formed at the point of uni
on of the two minor labia and covers the clitoris. The exposed part of the clito
ris is called glans clitoris.
The region between the labia minora is the vestibule within which are the hymen
(if still present), the vaginal orifice, the external urethral orifice and the o
penings of ducts of several glands. The vestibule is homologous to the membranou
s urethra of the males.
The ilioinguinal nerve and the genitofemoral nerves supply the mons pubis, the l
abia majora and the labia minora. Any of these structures may be involved in a c
hronic pain condition.
It is the vestibule, the vestibular glands and the labia which are frequently in
volved in vulvodynia.
Clinical presentation:
As mentioned earlier, vulvodynia may be Primary (or essential) and Secondary.
Primary vulvodynia is idiopathic, while the secondary form results from an infec
tion or some other known cause. Regardless of it being primary or secondary, vul
vodynia is described as a burning or aching sensation that is painful to touch.
Patients tend to wash or scratch the affected area, which leads to excoriations.

In localized vulvar pain syndrome, the pain is consistently and tightly localize
d by point-pressure mapping to one or more portions of the vulva, whereas in vul
var vestibulitis, the pain is localized by point-pressure mapping to one or more
portions of the vulval vestibule.
Vulvar vestibulitis is a painful condition that occurs when something is inserte
d into the vaginal opening, as done in tampon insertion or during sexual activit
y.
Dysesthetic vulvodynia is a painful condition that persists even in the absence
of touch or pressure. This is usually constant or triggered by light touch or a
normally non-painful touch. These findings are similar to complex regional pain
syndrome.
In a few patients, pain occurs or worsens before menses or after sexual intercou
rse. This is referred to as cyclic vulvitis. This may be a result of an infectio
n or an exaggerated reaction to hormone replacement therapy. These patients are
pain free during the rest of the month, a characteristic feature of this conditi
on.
Along with the features described above, patients usually tend to be depressed.
Depression is an effect, not a cause of the condition. The chronic nature of the
pain along with the inability to participate in or seek pleasure from sexual in
tercourse may lead to it. Depression manifests as a loss of interest in work, re
creation and sexual activity.
Women affected are usually nulliparous with a median age of 32 years. A few of t
he relatively common causes (of secondary vulvodynia):
Bartholin's abscess
Vulvovaginal candidiasis
Herpes
Herpes zoster
Human papilloma virus
Trichomonas and molluscum contagiosum infections
Trauma due to sexual assault, vaginal delivery, episiotomy, hymenectomy or vagin
al surgeries.
Diagnosis:
History and physical examination are of paramount importance in landing a diagno
sis when the patient presents to the doctor.
There are many testing modalities of pain and sensation that are useful in diagn
osing the condition and assessing the severity of the disease. Histological stud
ies reveal neural hyperplasia. A biopsy, though not pathognomic, reveals a low-g
rade chronic inflammatory picture consistently.
It is not easy to rule out infective causes, especially when the causative organ
ism is a fungus. Group B streptococcus and candida albicans are two of the commo
n causative agents of secondary vulvodynia.
Treatment:
Medical management:
This involves a multimodal approach and requires:
Antibiotic/Antifungal/Antiviral when the condition is secondary to an infection
Antihistaminics
Topical oestrogen
Sitz bath
Proper vulvar hygiene
Topical local anaethetics
Steroids
Anti-inflammatory agents
A few patients benefit from hormone replacement therapy, tricyclic anti-depressa
nts and anti-convulsants. That being said, there is an increasing school of thou
ght and evidence that suggests that it is of benefit to the patient to avoid oes
trogen and progesterone (used in hormone replacement) since there have been repo
rts implicating these agents in vulvodynia.
Abrasive washcloths, irritating cleansers and other irritants should be avoided.

Surgery:
Many surgical approaches have been suggested, tried and tested. These are usuall
y employed when the medical management fails to achieve pain relief. Procedures
include:
Pudendal nerve decompression
Resection of hymen and vestibule with mobilization of the lower vagina to cover
the defect.
Perineoplasty
Patient education:
Educating the patient about her condition is imperative. This may involve discus
sing the condition with the patient, trying to explain it to her in the most sim
plest of terms, giving her handouts, etc. Avoiding harmful habits such as scratc
hing or over cleansing the vulva should be stressed upon. Patient should be reas
sured of normalcy and the importance of maintaining a normal sex life, exercise
regimen and work routine should be elaborated.
Psycology:
Depression/Anxiety may be another after effect.
Cognitive-behavioral therapy
=
Urethral Pain Syndrome
Urethral syndrome is a term coined way back in 1949 by Powell and Powell. It is
a syndrome characterized by recurrent urethral pain, usually felt on voiding, da
ytime frequency, nocturia, with these symptoms of dysuria occurring without any
demonstrable evidence of infection. As a diagnosis, urethral syndrome or urethra
l pain syndrome or frequency-dysuria syndrome is a controversial and possibly an
obsolete term, in view of lack of clear diagnostic criteria and the overlapping
features with bladder pain syndrome (interstitial cystitis).
Diagnosis of Urethral pain syndrome is that of exclusion. This is especially tru
e since this entity occurs in the absence of infection and/or other obvious path
ologies. Historically, urethral stenosis was believed to cause urethral syndrome
. Current theories attempting to explain the cause of this painful syndrome incl
ude:
Hormonal imbalances
Inflammation of the Skene glands
Inflammation of the paraurethral glands
Environmental factors/ agents (examples: bubble bath, soaps, contraceptive gels,
condoms)
Hypersensitivity reaction following urinary tract infection (or to antibiotics t
aken for the infection)
Traumatic sexual intercourse
Irrespective of the inciting event, patients with urethral pain syndrome have bo
th involuntary spasms and voluntary tightening of the pelvic musculature during
each painful episode, which along with any residual injury or irritant, starts a
vicious circle of worsening dysfunction of the pelvic floor musculature.
In most of the cases, the initial cause of the pain has healed, but the pelvic f
loor dysfunction persists and is worsened by the patient's anxiety and frustrati
on with the condition.
This syndrome has a female predilection.
Clinical presentation:
Symptoms of Urethral syndrome
Urinary symptoms:
Increased frequency (every 30
60 minutes) with minimal nocturia
Supra-pubic discomfort, neither as much as nor as constant as that seen in inter
stitial cystitis
The patient often describes a sensation of constant urethral irritation rather t
han the searing discomfort with urination that is reported by patients with an a
ctive lower urinary tract infection.
Other Pelvic symptoms:

Associated bowel symptoms, menstrual cramps dyspareunia

Irregular or excessive menstruation
Sexual history:
Contraceptive methods (many contraceptive gels and condoms are irritative)
Sexual activity (rough intercourse, prolonged oral sex and intercourse in a heav
ily chlorinated hot tub or in a shower using bath soap as a lubricant may be the
etiology of urethral irritation) may elicit an etiology.
A history of sexual abuse has been linked with pelvic floor muscle dysfunction.
Habits:
Prolonged driving in vehicles with limited shock-absorbing mechanisms (eg, buses
, trucks)
Horseback riding
Long-distance biking
The above habits (among others) can result in urethral irritation.
Medication history:
It is important to rule out confounding factors through medication history such
as the use of diuretics (causing an increase in frequency) or the use of choline
rgic agents for cold (which can increase the tone of the bladder neck and the pr
oximal urethra)
Neurological symptoms:
Frequent falls, limping, or other neurologic symptoms may suggest a CNS abnormal
ity.
Multiple sclerosis usually presents in women at around the same age and must be
kept in mind at the time of the differential diagnosis
Physical examination:
A careful examination should be done to rule out any anatomical causes for the p
ain.
Urethral infections such as syphilis, gonorrhea, Chlamydia or mycoplasma stones,
tumours, cysts or diverticuli should be excluded.
Pain and tenderness may be present on palpation
Urethrocystoscopy may reveal slightly inflamed mucosa.
Differential Diagnosis:
The differential diagnosis may include:
Differential diagnosis:
Acute Bacterial Prostatitis
Anal fissure
Bacterial cystitis
Bladder cancer
Bladder stones
Cauda equine
Cervical cancer/ Cervicitis
Sexually transmitted diseases (Chlamydia, syphilis, gonococcal infection, etc.)
Chronic pelvic pain
Dysmennorhoea, Dysfunctional uterine bleeding, Endometriosis
Human papilloma virus
Neurogenic bladder, Bladder pain syndrome
Urethral cancer, urethritis, urethral strictures, urethral warts
Urinary tract infections
Vulvodynia
Treatment:
Treatment most commonly includes empirical antibiotic therapy followed by low-do
se long term antibiotic therapy.
The goal of treatment in urethral syndrome is to relieve the discomfort and urin
ary frequency. This often involves a trial-and-error approach, involving behavio
ral, dietary, and medical therapy.
The treating physician must gain the confidence of the patients and should provi
de assurance and encouragement throughout therapy.
Medications include hormone replacement (for women), anesthetics, antispasmodics
, tricyclic antidepressants (TCAs), muscle relaxants, and alpha-blockers.
Behavioral therapy, including biofeedback, meditation, and hypnosis, has been us

ed with some success.

Dietary therapy is directed primarily at increasing urinary pH.
Surgical Care
For a long time, the primary surgical procedure used to treat urethral syndrome
has been urethral dilation.
This is especially true in women with true urethral stenosis as the etiology of
their symptoms as they gain significant improvement after urethral dilation.
Implantable devices have been attempted to mildly stiulate the sacral nerve. The
se nerves provide the most distal common autonomic and somatic nerve supply to t
he pelvic floor, detrusor muscle, and lower gastrointestinal tract. In properly
selected patients, the stimulation by these implants can dramatically reduce or
eliminate symptoms.
Nd:YAG laser ablation of squamous metaplasia at the bladder neck-trigone has sho
wn some promise in patients with urethral syndrome refractory to medical managem
ent and with findings of trigonitis
=
Proctalgia Fugax
Proctalgia fugax forms one of the two major kinds of ano-rectal pain syndromes,
the other beingproctodynia, where the pain is continous.
"Proctalgia fugax represents a non-malignant pain syndrome of an unknown origin
that is characterized by paroxysms of rectal pain with pain free periods between
attacks."
Like seen in cluster headache, the disease may remit spontaneously and may last
for weeks to years. The pain of proctalgia fugax is limited to the anus and the
lower rectum.
Clinical Presentation:
Proctalgia fugax is more common in female patients. It is also commonly seen in
patients suffering from irritable bowel syndrome.
The pain in proctalgia fugax is sharp and gripping and is usually severe.
Stressful events tend to increase the severity and frequency of attacks. Sitting
for prolonged periods of time usually triggers an episode.
Patients usually proclaim a sense of an urgent need to defecate with the onset o
f the paroxysms of pain. Symptoms can be severe enough to limit the patient's ab
ility to carry out daily activity.
On physical examination, no overt abnormalities are usually found.
The patient may be depressed or appear anxious.
Rectal examination is usually normal but pain may be triggered on deep palpation
of the surrounding musculature.
Some patients report that the attack of pain may be stopped by placing a finger
in the rectum. Rectal suppositories may also abort the attacks.
Diagnosis:
Studies attempting to explain the pathological mechanism responsible for the pai
n in proctalgia fugax have implicated the spasm of the levator ani muscles, anal
sphincter and the sigmoid colon.
Proctalgia fugax is a diagnosis of exclusion and necessarily so since having a d
ocile approach may lead to missing an early/ timely diagnosis of a carcinoma.
Rectal examination is mandatory in all the patients who present with complaints
that may lead to the treating physician thinking of proctalgia fugax.
Sigmoidoscopy or colonoscopy is strongly recommended.
Testing of stool for occult blood is also an important step.
Other laboratory investigations include a complete blood picture, erythrocyte se
dimentation rate; blood chemistry (electrolytes, etc.) should be performed.
MRI scan or a CT scan of the pelvis must be considered if the diagnosis is in do
ubt.
Differential Diagnosis:
Rectal carcinoma
Proctitis
Haemorrhoids

Prostadynia
Treatment:
Many methods have been tried and tested and most of them directed at arresting t
he onset of pain. Many patients find that ingesting food immediately at the onse
t of the attack of pain helps in halting it altogether.
Digital dilatation or dilatation by administering enema or a rectal suppository
also ceases the attack of pain.
Initial treatment starts with a combination of simple analgesics and non-steroid
al anti-inflammatory drugs or cyclooxygenase-2 inhibitors. If pain still persist
s, then gabapentin or a tricyclic antidepressant may be added.
Tricyclic antidepressants have been the mainstay of treatment for many years for
the palliation of pain which results from proctalgia fugax. Unfortunately this
class of drugs is associated with a significant number of anti-cholinergic effec
ts which includes dry mouth, constipation, sedation, and urinary retention. The
use of these drugs should be done with caution especially in patients suffering
from
glaucoma, prostatism and cardiac arrhythmias.

TO encourage compliance, amitriptyline or nortriptyline at a 10mg bedtime dose.

The dose may be titrated to 20 m5 mg at bedtime .
Selective Serotoin reuptake inhibitors such as fluoxetine have also been used to
treat. These are better tolerated than the tricyclic agents, but less efficacio
us toward the pain of proctalgia fugax.
If the antidepressant drugs are unable to provide sufficient pain relief/ halt e
pisodes, Gabapentin should be started usually at a dose of 300 mg at bedtime for
2 nights. The drug is then increased in 300mg increments, given in equally divi
ded doses over 2 days until side effects allow and pain relief is achieved up to
a maximum dose of 2400mg per day is reached.
Local application of heat and cold may be beneficial to provide some pain relief
. The use of bland supplements may also help relieve the symptoms.
When all the above methods fail, the next option would be injection of the peron
eal nerves or caudal epidural nerve block with local anaesthetic and corticoster
oid.
There have been reports, albeit inconsistent, suggesting symptomatic reliefs wit
h calcium channel blockers, topical nitroglycerine and inhalational salbutamol.
A major problem in the care of these patients is the inadvertent oversight of an
y other pathology of the anus and/or the rectum, with the afflictions ranging fr
om infection to carcinoma. Early detection is important to prevent life-threaten
ing complications and to avoid the psychological damage resulting from the pain
involving the genitalia and the rectal region.
A note on the Levator ani Syndrome:
This syndrome is also referred to as Puborectalis syndrome or chronic proctalgia
or pelvic tension myalgia.
The symptoms which bring the patient to the physician are usually:
Dull aching or pressure like discomfort in the rectum lasting several hours.
Pain episodes are chronic and recurrent lasting for 20 minutes or longer.
Prolonged sitting and defecating trigger the pain
There is usually a sensation of incomplete defecation in most patients.
On examination, tenderness on palpation may be noted due to the levator muscle s
pasm. The tenderness is usually asymmetrical.
This too, like proctalgia fugax is a diagnosis of exclusion (look at the algorit
hm provided in the section on diagnosis above).
Treatment in most cases is symptomatic and involves digital massage to the levat
or ani muscle 3 to 4 times per week. Muscle relaxants such as benzodiazepines, m
ethocarbamol, etc. have been shown to be significantly useful. Sitz bath helps i
n some patients

Bladder Pain (Interstitial Cystitis)

Bladder pain syndrome/ interstitial cystitis is a clinical syndrome characterize
d by urinary urgency, frequency and pelvic pain of unknown etiology, present bot
h during the day and the night.
The European Society for study of Interstitial Cystitis (ESSIC) expands on this
definition and helps in classifying and defining bladder pain syndrome:
To use the name bladder pain syndrome (BPS), followed by a type indication; in a
transition period the name bladder pain syndrome/interstitial cystitis (BPS/IC)
could be used parallel with BPS
That BPS would be diagnosed on the basis of chronic (>6 months) pelvic pain, pre
ssure or discomfort perceived to be related to the urinary bladder accompanied b
y at least one other urinary symptom like persistent urge to void or frequency.
Confusable diseases as the cause of the symptoms must be excluded. Further docum
entation and classification of BPS might be performed according to findings at c
ystoscopy with hydrodistension and morphological findings in bladder biopsies. T
he presence of other organ symptoms as well as cognitive, behavioural, emotional
and sexual symptoms should be addressed.
That BPS type indications consist of two symbols: the first symbol corresponds t
o cystoscopy with hydrodistension and the second to biopsy: first symbols 1, 2 o
r 3 indicate increasing grade of severity at cystoscopy with hydrodistension sec
ond symbols A,B or C indicate increasing grade of severity of biopsy findings. X
indicates not done for both.
The table below is a classification, which also helps understand the nomenclatur
e using the symbols afore-mentioned:
This is a severely debilitating condition, with the etiology still remaining unc
lear. This condition is more common in women than in men. It is usually a result
of complex interactions between nervous, immune and the endocrine systems.
Though the intenational societies have reached a consensus on the definition of
bladder pain syndrome, the duration of the chronic pelvic discomfort hasn't stil
l been agreed upon. The American Urological Association uses similar definition,
but the period of chronicity of the bladder discomfort is =6 weeks, while other
societies tend to lead toward duration of = 6 months.
Despite the identification of this disease entity and it's existence in clinical
and research circles, thereby leading to extensive research, no specific clinic
al or urinary markers have been found and neither have any radiographic, laborat
ory or serological findings or specific biopsy patterns that may be pathognomic
have been reported.
Pathophysiology:
As indicated above, the pathophysiology of interstitial cystitis is poorly under
stood. Over time, many etiologies have been proposed in an attempt to explain an
d understand the pathogenesis, but have failed to encompass the various clinical
presentations, course and pattern of the disease progression or responses to th
erapies in a satisfactory manner.
Proposed etiologies of Interstitial Cystitis:
Effect of the mast cells on the detrusor and/or the mucosal layers of the bladde
r
Deficiency in the glycosaminoglycan layer on the luminal surface of the bladder
leading to increased permeability of the underlying submucosa to 'bladder-toxic'
substances
Production of toxic substance(s) in the urine
Neurogenic hypersensitivity
Locally mediated inflammation at the bladder or the spinal cord level
Pelvic floor muscle dysfunction leading to faulty voiding
Autoimmune disorder
That being said, clinically, the bladder pain syndrome is classified into two ty

pes:
Ulcerative or the classic type
Non-ulcerative or the Messing-Stamey type
Ulcerative type:
This is a classic presentation with a diffusely reddish appearance of the bladde
r surface epithelium associated with one or more ulcerative patches surrounded b
y mucosal congestion (termed as Hunner ulcer) on the lateral walls or on the dom
e of the bladder seen on cystoscopic examination.
Image from http://www.smithinstituteforurology.com/
Since discrete areas of mucosal scarring rupture during the procedure, these ulc
ers typically become apparent on the over distention of the bladder. Pain of the
ulcer may be present at the emptying of the urinary bladder, when the ulcerated
area comes in contact with other mucosal surfaces of the bladder.
Bladder biopsy shows that the ulcerative lesion is transmural, associated with m
arked inflammatory changes, granulation tissue, mast cell infiltration and in so
me cases, fibrosis. Over time, as the disease progresses, as a result of the fib
rosis, the bladder capacity gradually and progressively decreases.
Non-ulcerative type:
Symptoms are similar to the ulcerative type with the patients presenting with fr
equency, urgency and pelvic pain but the cystoscopic findings noted in the ulcer
ative type are absent here. On over-distention, these patients' bladders show 'g
lomerulations' that are discreet, tiny, raspberry-like lesions on the dome and t
he lateral walls of the bladder with tiny mucosal tears and submucosal haemorrha
ges. Biopsy findings are not significant, compared to those in classic type.
A look at the differential diagnosis and their exclusion:
Condition
Exclusion of the condition
Carcinoma
Cystoscopy and biopsy
Carcinoma in situ
Cystoscopy and biopsy
Infection with common interstitial bacteria:
Chlamydia trachomatis
Ureaplasma urealyticum
Mycoplasma hominis
Mycoplasma genitalium
Corynebacterium urealyticum
Mycobacterium tuberculosis
Candida species
Herpes Simplex
Human papilloma virus
Routine bacterial culture
Special culture
Special culture
Special culture
Special culture
Dipstick; if "sterile" pyuria culture for M. tuberculosis
Special culture
Physical examination
Physical examination
Radiation
Chemotherapy (including with cyclophosphamide) Medical history
Medical History
Bladder neck obstruction
Flowmetry and ultrasound
Neurogenic outlet obstruction Medical history, flowmetry and ultrasound
Bladder stone Imaging or cystoscopy
Lower ureteric stone
Medical history. If haematuria is present, then upper ur
inary tract imaging (CT scan or Intravenous pyelogram)
Urethral diverticulum Medical history and physical examination
Urogenital prolapse
Medical history and physical examination
Endometriosis Medical history and physical examination

Vaginal candidiasis
Medical history and physical examination
Cervical, uterine, ovarian cancer
Medical history and physical examination
Incomplete bladder emptying (urinary retention) Post-void residual urine volume
measured by ultrasound scanning
Overactive bladder
Medical history and urodynamics
Prostate cancer Physical examination and PSA levels
Benign prostatic obstruction
Flowmetry and pressure flow studies
Chronic bacterial prostatitis Medical history, physical examination, culture
Chronic non-bacterial prostatitis
Medical history, physical examination, c
ulture
Pudendal nerve entrapment
Medical history, physical examination, nerve blo
ck may confirm the diagnosis
Pelvic floor muscle related pain
Medical history, physical examination
It must be remembered that a confirmation of diagnosis of any of the above does
not rule out the possibility of bladder pain syndrome completely.
Treatment:
Treatment in most cases is started empirically.
Pentosan Polysulfate Sodium is the first oral drug developed for interstitial cy
stitis and was approved by the FDA in 1996. In clinical trials, the drug improve
d symptoms in 30 percent of patients treated. The exact mechanism of action is n
ot known but it has been reported that Pentosan polysulfate repairs the defects
in the mucosal and submucosal lining of the urinary bladder. The FDA-recommended
oral dosage of Elmiron is 100 mg, three times a day. Patients may not feel reli
ef from IC pain for the first 4 months. A decrease in urinary frequency may take
up to 6 months. Patients are urged to continue with therapy for at least 6 mont
hs to give the drug an adequate chance to relieve symptoms.
Aspirin and/or Ibuprofen are the first analgesics used in an attempt to relieve
the discomfort.
Some patients have reported benefit with the use of trycyclic anti-depressants (
AD) or antihistamines.
Weak (codeine) or strong opioids (morphine) are useful in providing some pain re
lied.
Intra-vesicle therapy is also beneficial. This is done with local anaesthetics,
heparin, hyaluronic acid, chondroitin sulfate, dimethyl sulfoxide, BCG and vanil
loids.
Transcutaneous electrical nerve stimulation (TENS): Mild electrical pulses can b
e used to stimulate the nerves to the bladder either through the skin or with an i
mplanted device. The method of delivering impulses through the skin is called tr
anscutaneous electrical nerve stimulation (TENS). With TENS, mild electric pulse
s enter the body for minutes to hours, two or more times a day either through wi
res placed on the lower back or just above the pubic area between the navel and th
e pubic hair or through special devices inserted into the vagina in women or into
the rectum in men. Although scientists do not know exactly how TENS relieves pel
vic pain, it has been suggested that the electrical pulses may increase blood fl
ow to the bladder, strengthen pelvic muscles that help control the bladder, or t
rigger the release of substances that block pain.
TENS is relatively inexpensive and allows people with IC/PBS to take an active p
art in treatment. Within some guidelines, the patient decides when, how long, an
d at what intensity TENS will be used. It has been most helpful in relieving pai
n and decreasing frequency in people with Hunner's ulcers. Smokers do not respon
d as well as nonsmokers. If TENS is going to help, improvement is usually appare
nt in 3 to 4 months.
Many patients have reported that smoking worsens the symptoms and hence must be
avoided.
Interventional procedures include:
o
Repeated bladder over-distention
o
Hypogastric/lumbar sympathetic blocks
o
Electromotive drug administration
o
Transurethral resection coagulation and Laser
remove the urothelial lesi
ons

o
o
?
?
?

Intravesical botulinum injection

anti-nociceptive
Surgery:
Supratrigonal cystectomy/Subtrigonal cystectomy/Radical cystectomy
Resection of ulcers
Bladder augmentation
Bladder training
Illustration for the diagnosis and treatment of Bladder pain syndrome/ interstit
ial cystitis

Coccydynia
Coccydnia or coccygodynia is a common pain syndrome characterized by pain locali
zed to the tailbone, which radiates to the lower sacrum and perineum. Simpson co
ined the term coccygodynia in 1859.
Image from http://houstonsportsmedicine.com/
It is seen more in women than in men. It usually occurs as a result of direct tr
auma to the coccyx from a kick or a fall onto the coccyx. It has also been noted
after a difficult vaginal delivery. Pain is usually a result of strain of the s
accrococccygeal ligament or sometimes a result of fracture of the coccyx. Arthri
tis is not a very common cause of coccydynia, but has been reported nevertheless
. Tumours affecting the coccyx or the surrounding soft tissue is another occasio
nal cause.
Many patients present with either subluxation or hypermobile coccyx. Coccygeal i
nstability leads to a state of chronic inflammation and pain. It is at least thr
ee times more common in obese patients compared to the non-obese ones. A look at
the common etiologies:
Etiology of Coccydynia:
Acute coccydynia:
Direct Trauma
Chronic coccydynia:
Damage to the sacrococcygeal ligament due to:
o
Difficult pregnancy
o
Difficult delivery
o
Repeated trauma
o
Repeated strain as a result of rowing, cycling or a faulty posture
Malformation of the coccyx:
o
Congenital
o
Degenerative bony spurs
Referred pain from damaged sacrum:
o
Cancer
Muscle strain or tension
Pinched nerves or damaged nerves
Dislocation of the coccyx
Clinical Presentation:
Patients with coccydynia complain of pain in and around the coccygeal area witho
ut significant low back pain or referred pain. Pain is typically associated with
sitting and is exacerbated on rising from a seated position. Patients may later
be affected with pain in standing or lying down position. Some patients complai
n of burning sensation in the rectal area associated with defecation, menstratio
n or sexual intercourse. Numbness is another common type of presentation, felt i
n the lower part of the spine. As a consequence of pain, patients may complain o
f depression, insomnia and exhaustion.
On physical examination the patient exhibits point tenderness over the coccyx. M
ovement of the coccyx may cause sharp paraesthesia to the rectum. On rectal exam

ination, the levator ani, piriformis and coccygeus muscles may feel hard and ten
se and the palpation of these muscles may result in the induction of severe musc
ular spasms. It may be noticed that when the patient sits in the out patient roo
m, he/she may be attempting to sit on one buttock to avoid severe pain.
Diagnosis:
Plain radiographs:
These are indicated in all patients who present with pain, which is thought to b
e arising from the coccyx, with the intention to rule out occult bone disease or
a tumour.
General Investigations:
Based on the patient's presentation, blood sampling is done for:
Complete blood picture, including ESR
Prostate-specific antigen
Anti-nuclear antibody
Further imaging:
Magnetic resonance imaging (MRI) is indicated if an occult mass/ tumour is impli
cated as the cause of the pain. Tc-99 bone scan may also be done, especially to
rule out conditions like chordoma. It also helps to rule out stress fractures th
at are easily missed by the plain radiographs. The injection technique serves as
both a diagnostic as well as a therapeutic manoeuver.
Differential Diagnosis
Primary infectious or inflammatory disease of the rectum and/or the anus
Primary tumours of the sacrum
Metastatic deposits
Proctalgia fugax (should be noted that here, movement of the sacrum doesn't caus
e pain)
Insufficiency fractures of the pelvis and sacrum
Disorders of the sacroiliac joint
Treatment:
Treatment of coccydynia may follow the following sequence:
Conservative therapy consists of
o
Simple analgesics: NSAIDs or cyclooxygenase-2 inhibitors
o
Foam donut to prevent irritation to the sacrococcygeal ligament
When the above fails, injection techniques are employed next:
o
The patient is placed in a prone position
o
The legs and heels are abducted to prevent tightening of the gluteal mus
cles (the tightening of these muscles makes the identification of the sacrococcy
geal ligament all the more difficult)
o
Prepare a wide area of skin with antiseptic solution.
o
Place a fenestrated drape to avoid contamination of the palpating finger
.
o
Palpate the joint at the base of the sacrum.
o
Use a 1.5inch, 25-gauge needle, insert through the skin in a 45-degree a
ngle into the region of the sacrococcygeal joint and ligament.
o
On penetrating the ligament, a "pop" will be felt; the needle should the
n be withdrawn. If bone is contacted, withdraw the needle slightly, this helps d
isengage the needle from the periosteum.
o
5 ml of 1.0% lidocaine (free of preservatives) and 40 mg of methylpredni
solone is slowly injected, after identifying the cerebrospinal fluid by withdraw
ing the plunger, thereby confirming the accuracy of the position.
A ganglion impar may be used in patients who do not respond to the above.
Coccydynia should be considered a diagnosis of exclusion in the absence of any h
istory of trauma. It is important that this disease be caught early, to avoid an
y disastrous consequences
Pudendal Neuralgia
Pudendal Neuralgia is a painful neuropathic condition, caused by the inflammatio
n of the pudendal nerve. The exact incidence of this ondition is not known, but
it is a genereal consensus that it is diagnosed significantly lesser when compar
ed to its actual existence. It is also referred to as "Alcock's syndrome" or "Pu

dendal canal syndrome".

Symptoms of Pudendal Neuralgia
Pain in the urogenital region (burning type of pain)
Altered skin sensitivity in the distribution of the pudendal nerve (genitals, pe
rineum, one third of the urethra and the rectum)
Urinary hesitancy, urgency, frequency, burning sensation
Pain during and/or after bowel movement
Pain during/after intercourse
Urinary and/or faecal incontinence
Pain in penis, scrotum, labia, vagina.
Men with so-called "abacterial prostatitis" or "prostatodynia" may indeed have P
udendal Neuralgia.
Also in men with pudendal nerve entrapment, aberrant development and subsequent
malpositioning of the ischial spine appear to be associated with athletic activi
ties during their youth. This is usually seen during the period of development a
nd ossification of the spinous process of the ischium.
Etiopathogenesis:
The exact mechanism of pudendal nerve dysfunction and damage, leading to perinea
l or pudendal neuralgia is dependent on its etiology.
An inflammatory response usually follows the pudendal nerve compression or entra
pment, which in turn leads to venous stasis, increase in vascular permeability a
nd eventually demyelination occurs. As a result, there is scar formation and in
cases where the inciting event is severe, permanent nerve damage occurs.
Neuronal function is impaired, instead of there occurring an inflammatory respon
se or demyelination, in patients with nerve tension injury. Pelvic floor dysfunc
tion itself may cause pain along the pudendal nerve distribution.
Diagnosis:
As in any other ailment, the road to diagnosis starts with history and physical
examination.
History is focused on describing the pain (its onset, duration, diurnal and post
ural variation, aggravating and relieving factors, trauma prior to onset of pain
, past medical and surgical history).
For these patients, the pain or other neurological dysfunction is described in a
ccordance with the distribution of the pudendal nerve. The patient may or may no
t give a history of common triggering factors (i.e. pelvic surgery, trauma, deli
very, etc.).
Patients will state that sitting increases symptoms and standing decreases sympt
oms to a certain extent.
On examination, altered skin sensitivity will be noted. This may either be hyper
- or hypoaesthesia.
Pressure on the pudendal trunk will produce pain (equivalent to Tinel's sign). T
his can be performed both transvaginally and transrectally.
A confirmation of this condition would be by using a pudendal nerve block, which
provides a near complete relief of pain for a few hours to a few weeks.
Electrophysiologic evaluation can help confirm the site of entrapment and the ty
pe of nerve damage. This includes EMG testing of the external sphincter, sacral
reflex, pudendal nerve terminal motor latency (PNTML) and somatosensory evoked p
otential studies.

A positive Tinel's sign and signs and symptoms of pelvic floor dysfunction are i
ndicative of nerve compression or entrapment as the etiology. When the pudendal
neuralgia is caused by nerve entrapment, physical therapy and injections alone a
re often not successful in completely eradicating the problem. In the event cons
ervative management is failing, sacral reflex testing is indicated to confirm or
rule out an entrapment.
Treatment:
Lifestyle modifications:
Avoiding activities, which worsen the condition such as sitting for prolonged pe
riods of time, cycling, etc, is a useful first step.
Sitting pads, especially those with cut outs to transfer pressure away from the
perineum can be used to provide some pain relief and the ability to continue wor
k unhampered.
Medical:
Analgesics have limited effect (including narcotics), since this pain is neuropa
thic in nature.
Tricyclic antidepressants and neuroleptic modulate the pain and have varying eff
icacy.
Nerve infiltration with a combination of a local anaesthetic and a corticosteroi
d or with heparin is effective in most cases. Multiple injections are usually re
quired, at least 3 to 5 with a 3 to 6 week interval between infiltrations.
Physical Therapy:
Perineum muscular dysfunction is one of the causative factors. Physical therapy
is thus useful in minimizing or eliminating the concurrent pain altogether.
Physical therapy is especially useful when the pain is triggered because of irri
tation of the pudendal nerve (trigger points: pelvic floor hypertonicity, myofas
cial trigger points, extrapelvic hypertonicity, adverse neural tension, sacroili
ac joint dysfunctions, etc.).
Special training is required for physical therapists to handle pudendal neuralgi
a.
The stress is usually on the strengthening of the pelvic floor.
Surgical:
Surgical techniques revolve around the decompression of the pudendal nerve. Pain
may persist after the procedure, or may be triggered by the above mentioned fac
tors and therefore post-operative physiotherapy is very important