Pheochromocytoma and Medical Malpractice

Pheochromocytoma is an adrenal gland tumor comprised of chromaffin cells that produce and release excess epinephrine and norepinephrine, which are hormones that effect heart rate, metabolism, and blood pressure. Pheochromocytomas are generally benign and can appear at any age; however, they commonly occur during middle age.

iStock_000017392233XSmall.jpgIf left untreated or unrecognized, this tumor can be life threatening. Researchers have yet to discover the underlying cause of pheochromocytoma. However, certain disorders such as Multiple Endocrine Neoplasia type II (MEN II), Von Hippel Lindau disease, Neurofibromatosis 1, and Familial Paraganglioma are associated with pheochromocytoma.

Isolated, paroxysmal episodes of hypertension occur in fewer than half of individuals with pheochromocytoma. Episodes of hypertension can occur at unpredictable intervals and usually last 15-20 minutes. During these episodes, the patient experiences hypertension, tachycardia, and fever; however, the patient’s vital signs can be normal at other times. As the tumor grows, episodes increase in frequency, length, and severity. Additional symptoms include abdominal pain, chest pain, irritability, pallor, and weight loss.

However, two thirds of patients experience chronic sustained hypertension. Whether sustained or episodic, the patient’s hypertension is associated with an increased risk of myocardial ischemia, heart failure, renal injury, and cerebrovascular accidents. Sudden cardiac death may occur secondary to catecholamaine-induced myocardial irritability and ventricular arrhythmias.

Diagnosis of pheochromocytoma is based on elevated levels of free catecholamines and metabolites, such as vanillymandelic acid and metanephrines, in the patient’s urine.  The following additional tests can be used to diagnose pheochromocytoma: abdominal CT scan, adrenal biopsy, catecholamines blood test, glucose blood test, metanephrine blood test, MIBG scintiscan, and MRI of the abdomen.

The current treatment for pheochromocytoma is surgery to excise the tumor. It is essential to stabilize the patient’s blood pressure and pulse with adrenergic blocking medication prior to surgery. When the tumor cannot be removed, medication is required to manage it. The majority of patients have benign tumors that are excisable; however, 10% of tumors recur and 25% of patients still have high blood pressure after surgery.

A medical malpractice lawsuit may arise when a patient presents with typical signs and symptoms of pheochromocytoma but the doctor fails to make the diagnosis thereby causing bodily injury, disability or death to the patient usually as a result of uncontrolled hypertension.

Wilson's Disease and Medical Malpractice

Wilson's disease is a rare autosomal recessive disorder, where copper accumulates in the body’s tissues and organs, specifically the liver, brain, and eyes. The body acquires and stores too much copper. Copper deposition causes damage, death, and scarring of tissues leading to dysfunction of organs. 

The incidence of Wilson’s disease is 1:300,000. If both parents possess an abnormal gene for Wilson’s disease, there is a 25% chance their child will have the disorder. The gene responsible for Wilson's disease is ATP7B. DNA testing is available for this gene; however, testing is complicated because different ethnic groups may have different mutations in this gene.

It is commonly seen in eastern Europeans, Sicilians, and southern Italians. Symptoms begin to present at age 4. Symptoms include abnormal posture of arms and legs, confusion or delirium, dementia, difficulty moving arms/legs, difficulty walking, emotional or behavioral changes, abdominal distention, personality changes, speech impairment, tremors of arms or hands, uncontrollable movements, hemoptysis, jaundice, etc.

Specific signs and tests are used to verify the diagnosis of Wilson’s disease. A slit lamp examination may demonstrate limited eye movement and Kayser-Fleischer rings, brown-colored rings around the iris. Physical examination may illustrate injury to the central nervous system such as loss of muscle control, coordination, memory, thinking and IQ. Other neurological signs may include muscle tremors and confusion.

In addition, the presence of liver or spleen disorders may be an indication for Wilson’s disease. Lab tests that assist in the evaluation for Wilson’s disease include: CBC, serum ceruloplasmin, serum copper, serum uric acid, and urine copper. If the patient possesses liver problems, one would expect to see the following picture: high liver enzymes (AST and ALT), high bilirubin, high PT and PTT, and low albumin. There are a myriad of other tests such as 24-hour urine copper test as well as abdominal and neurological imaging that can provide further evidence for or against the diagnosis.

Lifelong treatment is required to control Wilson's disease because it may cause fatal effects, such as loss of liver function and damage to the nervous system. In patients where the disorder is not fatal, symptoms may be disabling. The aim of treatment is to decrease the amount of copper in the body causing toxic effects.  Thus, medications known as chelators, which bind copper and remove it via the kidneys and guts, are utilized to treat this disorder. Unfortunately, certain medications that chelate copper, like penicillamine, can sometimes affect neurological function while others may not interfere with neurological function.

Also, a low-copper diet is recommended so individuals should avoid the following foods: chocolate, dried fruit, liver, mushrooms, nuts, and shellfish.  Individuals may want to drink distilled water because the majority of tap water flows through copper pipes. A liver transplant may be necessary in cases where the liver is severely damaged. In addition, people with severe neurological dysfunction may need special protective measures.

If left untreated, a variety of complications can result from Wilson’s disease including anemia, CNS damage, cirrhosis, liver necrosis, fatty liver, hepatitis, increased number of bone fractures and infections, jaundice, muscle atrophy, loss of ability to care for self and function independently, along with a number of other things. However, liver failure and injury to the central nervous system are the most common and dangerous effects. Wilson's disease is fatal if it goes undiagnosed and untreated.

Small Bowel Obstruction and Medical Malpractice

The small bowel is a long coiled hollow tube, called a tract, that is approximately twenty-five feet long. It includes the duodenum, jejunum and ileum.  A small bowel obstruction, also known as a small intestinal obstruction, is a mechanical or functional (paralytic) blockage of the intestinal tract, which prevents the normal transit of digestive products. It can occur at any level throughout the jejunum and ileum, and is considered a medical emergency when it occurs. The condition is often treated conservatively for the first several days; however, the patient must be monitored very closely for signs of clinical deterioration that can become life threatening.

iStock_000017493981XSmall.jpgMechanical obstruction is due to a mechanical barrier, such as an adhesive band from prior surgery, which creates a road block to the bowel.  On the other hand, functional obstruction is caused by an event that interferes with the nervous innervation of the bowel, such as electrolyte imbalances and metabolic disturbances. Functional bowel obstruction can be caused by a multitude of conditions whereas mechanical SBO is generally credited to a luminal, mural, or extra-mural mechanical barrier. A clinical syndrome exists called small intestinal pseudo-obstruction, which is characterized by manifestations of mechanical bowel obstruction in the absence of an obstructive lesion.

The symptoms of a mechanical small bowel obstruction include abdominal fullness and/or excessive gas, abdominal distention, pains and cramps in the stomach area (specifically the mid abdomen), vomiting, constipation (inability to pass gas or stool), diarrhea, and bad breath. Acute functional small bowel dilatation is referred to as adynamic or paralytic ileus. The symptoms of paralytic obstruction, in reference to the ileus, are abdominal fullness and/or excessive gas, abdominal distention, and vomiting after eating.  The pain less closely resembles the colicky type seen in mechanical obstruction, but may be just as severe

The diagnosis is determined by listening to the abdomen with a stethoscope. High-pitched, tinny and clanking sounds can be heard at the onset of mechanical obstruction.  If the blockage persists for too long or the bowel is significantly damaged, due to the stretching of the blood vessels supplying it thereby decreasing blood flow, bowel sounds will decrease and eventually become silent.  The hallmark of paralytic ileus is decreased or absent bowel sounds, which can create confusion in relation to the issue of etiology if this occurs.Diagnostic tests that demonstrate obstruction include plain radiographic film of the abdomen (usually in the flat and upright position), CT scan, barium enema and upper GI series with small bowel follow through

Treatment depends on the cause of the obstruction. In some cases, drastic measures are necessary to save a person’s life, while in others a strategy of watchful waiting is more appropriate. In general, more serious cases that require immediate treatment can be identified based on a patient’s vital signs and physical exam. If the person is very sick and appears to be on the brink of a serious event, surgery may be required to ensure the patient’s life.

To determine if there is any deterioration consistent with lack of blood flow, which leads to bowel ischemia, gangrene, perforation, septic shock, and death, it is imperative that the following steps be taken. The bowel must be decompressed with a long indwelling tube, all oral feeding must be stopped and IV therapy must be initiated with continuous monitoring and observation. There is no reason anyone presenting to the emergency room with a small bowel obstruction should die in the hospital.

Sigmoid Colon Volvulus and Medical Malpractice

The term volvulus is derived from the Latin word volve, which means to twist. A colonic volvulus occurs when a part of the colon twists on its mesentery, resulting in acute, subacute, or chronic colonic obstruction.  Volvulus involving the sigmoid colon is the most common, occuring in 75% of cases.  Sigmoid volvulus occurs when the last part of the large bowel just before the rectum (named for its “S” shape) twists on its self.  It is common in elderly men, but it is likely to occur in anyone with a redundant sigmoid colon. 

More than 60-70% of patients present with acute symptoms; the remainder present with subacute or chronic symptoms. A history of chronic constipation is common. The patient may describe previous episodes of abdominal pain, distension, and obstipation suggestive of repeated, subclinical episodes of volvulus.  With continued obstruction, nausea and vomiting can occur. The development of constant abdominal pain is ominous. It indicates there may be a closed loop obstruction with significant intraluminal pressure, which can lead to ischemic gangrene and bowel wall perforation.

Abdominal distension is generally massive and characteristically tympanitic over the gas-filled, thin-walled bowel loop. The presence of overlying or rebound tenderness raises the concern of peritonitis due to ischemic or perforated bowel. A patient with a history of acute volvulus episodes that spontaneously resolve can experience marked distention with minimal abdominal pain.

A radiographic film of the abdominal will demonstrate a huge air filled distended bowel frequently in the shape of an inverted “U,” with the convexity of the “U” facing the right upper abdominal quadrant.  A barium enema will show dilation in the sigmoid colon due to a twist. A physician may refer to an area of complete obstruction with some twisting as the “bird beak” sign.

CT scans can demonstrate crossing sigmoid transitions, tagged the X-marks-the-spot sign, and folding of the sigmoid wall by partial twisting, called the split-wall sign.  However, the most sensitive finding on CT is a sigmoid colon transition point, which is seen in 95% of scans, and a disproportionate enlargement of the sigmoid colon, noted in 86% of cases.

Colonoscopy or flexible sigmoidoscopy could be done to both confirm the diagnosis as well as attempt to treat the obstruction. Barium enemas can also reduce the obstruction when the pressure of the fluid rushing into the bowel unwinds it.

For treatment, the first step is to free the acute obstruction, and then to fix the redundant part of the bowel to prevent reoccurrence.  In up to 90% of patients with sigmoid volvulus, the condition recurs after untwisting with methods as noted above. For this reason, anyone with a sigmoid volvulus needs to undergo an operation during the same admission to either remove or fix down the excessive bowel length.

Once the diagnosis of sigmoid volvulus is confirmed, treatment must be immediate. A delay in treatment represents a greater likelihood of bowel wall death and gangrene. Up to 80% of people with this condition die from gangrene if intervention is delayed. In the event this diagnosis is missed and bodily injury results, the treating health care provider is at risk of a medical malpractice lawsuit.

Triple Negative Breast Cancer and Medical Malpractice

By dividing breast cancer into molecular breast cancer subtypes, physicians and researchers can devise better approaches and treatments for dealing with the disease. Most studies divide breast cancer into four major molecular subtypes: Luminal A, Luminal B, Triple-negative, and HER2/neu. Triple-negative breast cancer is characterized by tumors that lack estrogen, progesterone, and human epidermal growth factor receptors

iStock_000018505784XSmall.jpgHigher rates of triple negative breast cancer have been recorded in younger women, Hispanic and African American women, and women of lower socioeconomic class. Triple negative cancer tends to have a poorer prognosis than other types of breast cancer that have more available and effective treatments.

Studies have demonstrated that triple-negative breast cancer possesses a higher probability for recurrence and spreading beyond the breast. This risk is greater within the first few years post-treatment but over time the risk becomes similar to other types of breast cancer. In addition, triple-negative tends to present as a higher grade cancer, meaning that a greater number of cancer cells are abnormal in appearance

Although surgical and radiation treatments are similar for different types of breast cancer, drug treatments usually vary. Many therapies for breast cancer target cellular receptors. A receptor is a molecule generally located on the surface of cells that is involved with chemical signaling. When a molecule binds to a receptor, it causes the cell to perform certain actions such as division or multiplication. Targeted drug treatments like tamoxifen or Herceptin, designed to treat HER2 positive breast cancer, have not been developed for triple negative. A patient with triple-negative does not express estrogen, progesterone, and HER2/neu receptors so therapy against these receptors is ineffective.

Standard treatment for triple-negative breast cancer is chemotherapy. Current treatments include anthracylines, taxanes, ixabepiplone, platinum agents, and biologic agents. Patients undergoing chemotherapy can experience side effects such as vomiting, nausea, alopecia, mucositis, myelosuppression, etc. Surgery and radiation are additional avenues of treatment. Currently, cancer experts are studying several promising drug strategies targeted for triple negative breast cancer such as PARP inhibitors. 

Septic Arthritis and Medical Malpractice

Septic arthritis, also known as reactive arthritis and bacterial arthritis, is inflammation of a joint caused by infection. When it develops, it represents a medical emergency. It develops when bacteria or fungus is transmitted through an individual's bloodstream to a joint. Individuals can develop septic arthritis at any age but it is less common between the ages of three to adolescence.

The majority of acute cases involve bacteria such as staphylococcus or streptococcus. However, children who develop septic arthritis tend to be infected with Group B streptococcus or Haemophilus influenza, if they have not been vaccinated. The number of cases that progress to a chronic infection are less common. Chronic infections are generally caused by organisms such as Mycobacterium tuberculosis and Candida albicans.

Overall, the most common sites of infection are the hip and knee joints. The following are considered risk factors for septic arthritis: artificial joint implants, bacterial infection, chronic disease (diabetes, rheumatoid arthritis, and sickle cell disease), intravenous drug use, immunosuppressive medications, and recent joint surgery or arthroscopy.

Septic arthritis generally presents with a rapid onset of symptoms. Patients develop a fever in addition to joint swelling, redness, and pain in the infected joint. Patients may also experience pseudoparalysis, which is an inability to move the extremity possessing the infected joint. To diagnose septic arthritis, physicians will aspirate the joint fluid to check the cell count, look for crystals under the microscope, and perform a gram stain and culture. In addition, other tests include a blood culture and an X-ray of the affected joint.

Possible complications include joint degeneration and permanent joint damage, which can occur if appropriate treatment is delayed. If antibiotics are promptly given to treat the infection the patient has a good prognosis. If fluid accumulates in the joint, aspiration may be necessary. Aspiration involves a needle being inserted into the joint to drain off the excess fluid. Only severe cases require surgery to remedy the infected joint fluid; however, if a prosthetic joint is affected, it may need to be replaced

Normal Pressure Hydrocephalus and Medical Malpractice

iStock_000015502953XSmall.jpgCerebrospinal fluid (CSF) is a clear fluid that surrounds the brain and spinal cord. This fluid is continually produced and stored in ventricles, which are cavities of the brain. CSF cushions the brain, supplies the brain with nutrients, and removes wastes.  Excess fluid drained from the brain is absorbed by other tissues.

Hydrocephalus is a condition in which there is an abundance of CSF in the ventricles due to interference in proper drainage and absorption. To accommodate the extra fluid, the ventricles enlarge causing compression of  different parts of the brain.

Normal pressure hydrocephalus (NPH) is a type of hydrocephalus that occurs commonly in older adults. NPH is different from other types of hydrocephalus because it develops gradually. The slow enlargement of the ventricles causes the fluid pressure in the brain to not be as high as in other types of hydrocephalus. However, the enlarged ventricles still press on normal brain tissue

NPH often presents with the following clinical triad of findings: urinary incontinence, gait disturbance, and dementia, with urinary symptoms appearing later in the sequence.  Gait disturbance is often the initial and most prominent symptom of the triad. It may be progressive due to the expansion of the ventricular system. It generally presents as unsteadiness or impaired balance. Eventually, gait disturbances can lead to a need for canes or walkers. An increased tendency to fall backwards is also common. In the very late stages, the patient can progress to an inability to stand, sit, and rise from a chair. 

Dementia presents as apathy, forgetfulness, and a dullness of thinking. Memory problems are often predominant, which can contribute to a misdiagnosis of Alzheimer's disease. Although recall is severely impaired in NPH, recognition, a hallmark of Alzheimer’s, is either normal or slightly impaired.

Idiopathic NPH is normal pressure hydrocephalus occurring without a known cause; however, it can be attributed to any condition that blocks the flow of CSF such as bleeding from an abnormal blood vessel, an aneurysm, a closed head injury, meningitis or similar infections, and surgery on the skull.

The diagnosis of NPH is made by performing a lumbar puncture (spinal tap). If the initial pressure measurement is elevated, it points to a diagnosis of NPH. Clinical improvement after removal of CSF has a high predictive value for treatment success.  A CT scan of the brain will show enlarged ventricles, and an MRI may show certain technical findings consistent with enlarged ventricles and elevated cerebral pressures. Imaging alone cannot differentiate between NPH and other dementia causing conditions such as Alzheimer’s disease, Atherosclerotic vascular disease, and Parkinson’s disease.  

Treatment for NPH is surgical diversion of the excess CSF. A shunt is implanted to drain CSF from the intracranial ventricular system to a different location such as the peritoneal space in the abdomen. The most common shunts utilized today are called the ventriculoperitoneal (VP) and ventriculoatrial (VA) shunts.  Placement of a shunt is a neurosurgical procedure performed under general anesthesia, and usually takes less than an hour to complete. Cognitive impairment associated with dementia has been reported to improve in more than fifty percent of cases. Successful treatment for NPH is available; therefore, it is medicaly negligent to misdiagnose NPH as Alzheimer’s dementia, where responses to the latest therapy innovations are only temporary.   

Hydrocephalus and Medical Malpractice

Hydrocephalus is also known as "water in the brain."  It is a condition in which there is an abnormal accumulation of cerebrospinal fluid (CSF) in the ventricles, which are cavities in the brain.  In infants with hydrocephalus, CSF builds up in the central nervous system, causing the soft spot near the front of the scalp, known as the anterior fontanelle, to bulge and the head to be larger than expected. There is also a soft spot near the back of the head known as the posterior fontanelle. Early symptoms may include sundowning, which is when the eyes appear to gaze downward; irritability; seizures; separated scalp sutures; sleepiness; and vomiting.

In newborns with hydrocephalus, the head circumference rapidly enlarges and may surpass the 97th percentile when measured at pediatric visits.  If the skull bones have not yet firmly joined together at this age, bulging, firm anterior and posterior fontanelles may be present when the patient is in an upright position. The infant may exhibit fretfulness, poor feeding, and frequent vomiting.

As the hydrocephalus progresses, torpor, a state of sluggishness and reduced metabolism, sets in and the infant shows lack of interest in his/her surroundings. In a later stage, the upper eyelids become retracted and the eyes turn downwards (due to hydrocephalic pressure on the mesencephalic tegmentum and paralysis of upward gaze). Movements become weak and the arms may become tremulous.  There may be reduction of vision. Over time, the head becomes so enlarged that the growing child becomes bedridden and he/she is unable to lift or even move this huge object attached to its neck.

Hydrocephalus is diagnosed through clinical neurological evaluation and by using cranial imaging techniques such as ultrasonography, computed tomography (CT), magnetic resonance imaging (MRI), or pressure-monitoring techniques. The most common initial diagnostic test to determine hydrocephalus is an image of the brain (CT Scan or MRI) to identify the enlarged ventricles (spaces) within the brain that are typical of hydrocephalus.  

Hydrocephalus is often treated with the surgical placement of a shunt system. This system diverts the flow of CSF from a site within the central nervous system (CNS) to another area of the body where it can be absorbed.  A shunt is a flexible but sturdy tube composed of silicone and plastic.   A shunt system consists of a shunt tube, a catheter, and a valve. One end of the catheter is placed into one of the dilated a ventricles inside the brain.  Depending on the situation, it could also be placed into a cyst or somewhere near the spinal cord. The other end of the catheter is usually placed within the abdominal cavity.  It could also be placed into any area, such as the heart, where the extra cerebrospinal fluid can be drained and absorbed.  The valve located along the catheter maintains one-way flow and regulates the rate of CSF flow.

Hydrocephalus can be effectively treated with a shunt; however, there is still a potential for complications. The shunt can become blocked. Symptoms of blockage include headache and vomiting. There may be other problems with the shunt such as kinking, tube separation, or infection in the area of the shunt. Other complications may include infections such as meningitis or encephalitis, intellectual impairment, and nerve damage.  Untreated hydrocephalus has a 50-60% death rate. Survivors have varying degrees of intellectual, physical, and neurological disabilities.  

Deep Venous Thrombosis and Medical Malpractice

Deep venous thrombosis is the development of a blood clot in the large, deep veins of the lower leg and thigh. Thrombi can cause tissue injury due to vascular occlusion or distal embolization. However, venous obstruction can be offset by collateral blood vessels. Thrombi can also cause local pain and edema due to the blockage of blood flow. If the clot breaks off and travels through the blood, it is referred to as an embolism. An embolism can become trapped in the brain, lungs, or heart leading to major injury. Pulmonary embolus (PE) is a common complication and life threatening if not treated quickly with anticoagulants. PE presents with shortness of breath, chest pain, and cough with blood in sputum

iStock_000012053156XSmall.jpgDVT can occur with stasis or in hypercoaguable states. It is commonly seen following trauma, surgery, or burns, which contribute to decreased physical activity, damage to vessels, and release of procoagulant substances from tissues. Reduced physical activity causes a decline in the milking action of lower leg muscles and slows venous return. Risk factors for DVT include advanced age, bed rest, immobilization, smoking, birth control pills, family history of blood clots, fractures in the pelvis or legs, giving birth within the last 6 months, heart failure, and obesity.  To prevent DVT, patients should move their legs during long flights or when they are immobile for long periods of time.

Although many DVTs are asymptomatic, they can recur. Some individuals suffer from post-phlebitic syndrome, which involves chronic pain and swelling in the leg. The major symptoms of DVT include changes in a patient’s leg such as redness, increased temperature, pain, and tenderness. Diagnosis is based on the physical exam, which should demonstrate a red, swollen leg. Diagnostic tests include a D-dimer blood test along with other blood tests to check for hypercoagulability such as activated protein C resistance, anti-thrombin III levels, antiphospholipid antibodies, and genetic testing for mutations with a predisposition towards blood clots. Imaging studies of the legs include Doppler ultrasound, plethysmography, and radiography.

The primary treatment for DVT is anti-coagulants, also known as blood thinners. They prevent the formation of new clots and the growth of old clots. However, they cannot dissolve existing clots. Patients are more likely to bleed on these medications. Heparin is an IV administered anticoagulant given in a hospital setting.  Warfarin (Coumadin) is an oral anticoagulant that takes several days to work; thus, Heparin cannot be stopped until Warfarin is functioning at an effective dose for a minimum of two days. Many patients wear pressure stockings on their legs to improve blood flow and decrease their risk of DVT.  When medications are ineffective, patients may need to undergo surgery. A filter can be placed in the body’s largest vein to prevent thrombi from migrating to the lungs. Also, surgery may be necessary to remove large thrombi.  

Pituitary Adenomas and Medical Malpractice

A pituitary adenoma is generally a benign, slow growing tumor that occurs in the pituitary gland. The pituitary gland is a small, bean shaped structure that lies at the base of the brain. It has a central role in the regulation of hormones that affect the body such as Adrenocorticotropic hormone (ACTH), Growth hormone (GH), Prolactin, and Thyroid-stimulating hormone (TSH).

Approximately 1 in 1,000 individuals have pituitary adenomas. They are generally not cancerous but may invade nearby structures.  They are classified based on size. A microadenoma is less than 1 cm in diameter whereas a macroadenoma is larger than 1 cm in size.

iStock_000017548218XSmall.jpgBased on whether the pituitary adenoma is a hormone-producing or hormone-inactive tumor, the patient will present with different symptoms. Hormone-producing tumors will make excessive amounts of an active hormone so symptoms present as a hormonal imbalance. The three most common hormone-producing adenomas are Prolactinomas, Growth hormone-secreting pituitary adenoma, and ACTH-secreting pituitary adenoma.

If the patient has a large hormone-inactive or hormone-producing tumor, it may compress surrounding brain structures due to its size.  Large pituitary tumors may compress the pituitary gland contributing to pituitary failure, which can lead to sexual dysfunction, inadequate body cortisol levels, and hypothyroidism. Other possible presentations relating to compression of brain structures include visual loss, headache, the “stalk effect”, and pituitary apoplexy.  The “stalk effect” is due to the compression of the pituitary stalk, the structure connecting the brain to the pituitary gland, which leads to a mild elevation in the hormone prolactin. Higher levels of prolactin in females can contribute to irregular menstrual cycles. Pituitary apoplexy presents with an abrupt headache and visual loss. It can occur under two different situations. The pituitary adenoma can bleed internally causing a sudden increase in size or the tumor can outgrow its blood supply and the dead tissue will swell.

Pituitary adenomas can be diagnosed based on endocrine function testing, imaging, and visual field testing. Often times, visual problems may be the only symptom present.  Optometrists and ophthalmologists should seriously consider the possibility of a pituitary tumor when the patient presents with an unexplained loss of visual field (especially peripheral vision), double vision, or blurred vision as the growth of a pituitary tumor can cause compression on the visual pathway (retina, optic nerve, etc). A delay in diagnosis of a pituitary adenoma may result in permanent loss of vision due to the damage caused by this compression. Endocrine function testing evaluates cortisol, follicle-stimulating hormone, lutenizing hormone, insulin growth factor-1, prolactin, testosterone/estradiol, and thyroid hormone levels. The preferred method of imaging is MRI, which screens for adenomas larger than 4 mm.

Treatment for pituitary adenomas depends on the presence of hormone production, size of the tumor, invasion of the tumor into surrounding structures, and the age and health of the patient. Drug therapy is used to treat hormone-producing tumors. For example, bromocriptine and cabergoline are used to treat tumors secreting prolactin because these medications decrease prolactin levels and tumor size. Pituitary adenomas that require surgery are usually minimally invasive techniques, where the tumor is removed through the nose.  On the other hand, radiation therapy involves high doses of radiation being delivered to the tumor. It is a treatment utilized for pituitary adenomas that cannot be controlled by drug therapy or surgical intervention. Patients have the best outlook when the entire tumor can be removed.