Halitosis and Other Breath Odors

What are the various causes of bad breath and how can they be recalled with ease? The best method is to visualize the respiratory and upper gastrointestinal (GI) tree, because this is where the substances (mucus, sputum, and vomitus or regurgitant material) that produce these odors may be found.

In the mouth, pyorrhea due to poor dental care and infection may cause halitosis. A stomatitis (e.g., aphthous) may also be a cause. Sinusitis and atrophic rhinitis are causes in the nasal passages. Anyone who has a friend with large tonsils knows that this is a frequent cause, especially when the tonsils become infected. Any form of pharyngitis may also cause halitosis. Carcinoma and tuberculosis (TB) of the larynx and lower respiratory tract may cause halitosis. More likely causes are bronchiectasis and lung abscess.

Proceeding down the esophagus to the stomach, one should recall the accumulation of food in diverticula, cardiospasm of the esophagus, and the frequent foul odor of chronic membranous or granulomatous esophagitis associated with a hiatal hernia. Carcinoma of the esophagus may also cause obstruction and allow putrefaction of food that accumulates there. A chronic gastritis or gastric carcinoma may also cause halitosis.

A sweet odor to the breath may be found in diabetes mellitus and alcoholism. Uremia will often present with an ammoniac and urinous odor to the breath, whereas the breath of hepatic coma may be fishy (fetor hepaticus). The feculent odor of a gastrocolic fistula and late states of intestinal obstructions should also be recalled. A garlic odor is found in many poisonings (arsenic, organophosphates, etc.).

Approach to the Diagnosis

The workup of bad breath involves a careful examination of the mouth and nasal passages. If this is negative, chest and sinus x-rays and upper GI series with barium swallow should be done. If the studies are still unrewarding, then endoscopy of the respiratory and upper GI tract would be indicated. Appropriate liver and renal function tests will be ordered when uremia or hepatic coma is suspected. If pyorrhea is suspected, refer the patient to a dentist.


A hallucination is seeing, hearing, touching, smelling, or tasting something that is not there. Auditory hallucinations without evidence of mental deterioration usually indicate schizophrenia, but epilepsy, drug toxicity, and brain tumors must be excluded. Visual hallucinations are often the sign of drug or alcohol intoxication, but occasionally they occur in schizophrenia. Hallucinations with mental deterioration should prompt the recall of the differential diagnosis for memory loss (see page 295). When faced with a hallucinating patient, think of the mnemonic MINT, and a list of possibilities can be recalled easily.

  • M—Mental disease brings to mind schizophrenia, manic depressive psychosis, and paranoid states.

  • I—Intoxication and inflammation suggest alcoholism, cannabis, lysergic acid diethylamide, bromism, various other drugs, and encephalitis, cerebral abscess (temporal lobe especially), and syphilis. The I should also suggest idiopathic disorders such as epilepsy, presenile dementia, and arteriosclerosis.

  • N—Neoplasm suggests brain tumors. A tumor of the occipital lobe may present with visual hallucinations, whereas a tumor of the temporal lobe causes auditory hallucinations or uncinate fits (i.e., bad smells). A tumor of the parietal lobe may present with tingling or other paresthesias of the body.

  • T—Trauma should suggest concussions, epidural or subdural hematomas, and depressed skull fractures.

Approach to the Diagnosis

In the workup of hallucinations, it is essential to get a drug history from a relative or friend if not from the patient. Ask about a family history of epilepsy or head trauma. A drug screen should be ordered. If there is no mental deterioration, referral to a psychiatrist may be done but an electroencephalogram (EEG) may still be indicated. A therapeutic trial of 100 mg of thiamine IV should be done if Wernicke encephalopathy or Korsakoff syndrome is suspected. With mental deterioration, a neurologist should be consulted. When there is doubt about mental deterioration, psychologic testing may be done. Computed tomography (CT) or MRI scans, EEGs, skull x-ray films, and arteriograms may be necessary in selected cases.

Hand and Finger Pain

Visualize the anatomy when a patient presents with pain in the hand or fingers (Table 31). The skin may show contact dermatitis, fungal infection, furuncle, cellulitis, or traumatic lesion. An insignificant wound may be infected; if there are streaks going up the arm, lymphangitis has complicated the picture. Herpes zoster rarely occurs in this area. Underneath the skin, the many tendon sheaths and fascial pockets are inviting sites for infection following a minor wound, but the swelling is obvious. One space particularly well known, the pulp space at the tip of the finger (usually the index finger), may develop a felon. A paronychial infection that involves the nail is very painful. A hematoma under the nail is perhaps even more painful.

Halitosis and other breath odors.

The arteries of the hand may go into intermittent painful spasms in the Raynaud phenomenon, which occurs, for example, in macroglobulinemia, menopause, and rheumatoid arthritis (RA). It also occurs in a primary form called Raynaud disease. This is an extremely painful condition associated with cold, blue hands (intermittently) and gangrene (ultimately). The collagen diseases and Buerger disease may cause a vasculitis of the arteries and the Raynaud phenomenon. Finally, peripheral arterial emboli may occur here, but they are more frequent in the lower extremities.

Surprisingly, the veins of the hand do not frequently develop thrombophlebitis, except in the hospitalized patient on frequent intravenous therapy. This may not be
unusual when one realizes that varicose veins are uncommon in the upper extremities. Buerger disease also may involve the veins of the hand. The tendons are sometimes trapped in their sheaths and cause pain. De Quervain stenosing tenosynovitis of the extensor pollicis tendon is a common form. Ruptured tendons of the fingers such as mallet finger should be obvious. The muscles of the hands are not commonly involved in myositis but are frequently traumatized and contused, particularly in contact sports.

Halitosis and other breath odors.

Trapping of the median nerve in the carpal tunnel is a well-known cause of pain in the hand and fingers, particularly in the thumb, index, and middle fingers. Sensory changes involve these and the medial half of the ring finger; there may be significant atrophy of the thenar eminence with the Tinel sign. The Phalen test is usually positive also. Remember that the ulnar nerve may be trapped in Guyon canal also, causing pain in the little finger and associated sensory changes. The carpal tunnel syndrome may be caused by multiple myeloma, amyloidosis, acromegaly, RA, menopause, and a host of other conditions.

Symptoms similar to those of the carpal tunnel syndrome may come from high up the peripheral nerve tract. Compression of the brachial plexus by a cervical rib, a scalenus anticus muscle, or the clavicle (so-called costoclavicular compression syndrome) may be the culprit. Chronic bursitis or arthritis of the shoulder may ultimately lead to a causalgia, as will a peripheral nerve injury, and create pain in the hand and fingers. The frozen shoulder following pneumonia, myocardial infarctions, and other chest conditions can do the same. The brachial plexus may also be involved by Pancoast tumors.

At a third site, compression of the cervical nerve roots by a herniated disc, cervical spondylosis, TB, and primary and metastatic tumors may be the cause of hand and/or finger pain. Cord conditions like syringomyelia and

brain stem involvement of the thalamus by embolism or thrombosis may occasionally cause pain in the hand, but in the latter condition, there is usually an accompanying leg pain.

Table 31 Hand and Finger Pain

Degenerative and Deficiency
Autoimmune Allergic
Skin Periarteritis nodosa
Herpes zoster
Carcinoma       Contact dermatitis
Erythema multiforme
Fascia, Ligaments, Tendon Sheaths, Subcutaneous Tissue   Felon
Tendon sheath infection
Sarcoma   De Quervain stenosing tenosynovitis Ganglion Scleroderma Hematoma
Ruptured tendon
Arteries Arteriosclerosis
Norwegian pulseless disease
Subacute bacterial endocarditis Macroglobulinemia     Buerger disease Vasculitis
Rheumatoid arthritis
Veins   Thrombophlebitis       Buerger disease      
Muscles   Myositis              
Peripheral Nerves (Carpal Tunnel)   Multiple myeloma       Amyloidosis
Rheumatoid arthritis
Diabetes mellitus
Brachial Plexus Ischemic neuritis
Myocardial infarction
Pancoast tumor   Scalenus anticus syndrome Cervical rib   Costoclavicular compression  
Spinal Cord and Cervical Roots   Tuberculosis Primary or metastatic tumors of cord Cervical spondylosis
    Rheumatoid spondylitis Herniated disc
Bone   Gonococcal arthritis   Osteoarthritis Gout   Rheumatoid arthritis
Lupus erythematosus

Hand and finger pain.

In the deepest penetration of our dissection of the hand, we encounter the most common structures that cause hand pain, the bones and joints. The bones may be fractured, dislocated, or contused or the joints may be sprained, but if the joints are painful, arthritis is the most likely cause. This may be RA, osteoarthritis, gout, or gonococcal arthritis. More rarely, it is associated with psoriatic arthritis, lupus erythematosus, and other systemic diseases.

Approach to the Diagnosis

In diagnosis, most of these conditions will be obvious on inspection. The difficulty arises when the hand looks normal. Then one must check for the following:

  • Carpal tunnel syndrome by tapping the volar aspect of the wrist (Tinel sign)

  • Brachial plexus neuralgia and scalenus anticus syndrome by Adson tests

  • Causalgia by stellate ganglion block to see if pain is relieved

  • Cervical spine disease by a roentgenogram, possibly a myelogram or magnetic resonance imaging (MRI), and nerve blocks of the various roots. Referral to a neurologist is often necessary. In early RA, the joints may be normal on inspection, but pain and stiffness of the hands and fingers in the morning is an excellent clue.

  • Pain over the radial aspect of the wrist which is aggravated by flexing the thumb and applying ulnar deviation is most likely de Quervain tenosynovitis. This is called the Finkelstein test.

  • Tenderness in the anatomical snuffbox may indicate a scaphoid fracture. A plain x-ray may be normal and only a bone scan will demonstrate the fracture.

Other Useful Tests

  • Arthritis panel

  • Antinuclear antibody (ANA) test (lupus erythematosus)

  • Electromyogram (EMG) and nerve conduction velocity (NCV) test (carpal tunnel syndrome)

  • X-ray of hand (arthritis)

  • Cold response test (Raynaud phenomenon)

  • Muscle biopsy (collagen disease)

  • Serum protein electrophoresis (macroglobulinemia, multiple myeloma)

  • Exploratory surgery

  • Nail fold capillary loop dilatation and dropout (Raynaud disease)

  • Therapeutic trial of a steroid and Xylocaine injection (carpal tunnel syndrome)


This symptom is best analyzed by using anatomy, as seen in Tables 32 and 33, but differentiation by pathophysiology is interesting, particularly in muscle traction headaches and migraines.

Moving by layers from the skin to the center of the brain is the local application of the anatomic process. Thus, sunstroke is a cause of headache originating in the sunburnt skin, as is herpes zoster. Abscesses of the scalp are uncommon but significant causes of head pain. Moving to the muscles, one encounters the most common cause of headache, muscle traction headache, which may be secondary to other conditions (e.g., migraine or eyestrain), or primarily due to nervous tension or constantly holding the head in one position. Fibromyositis (usually of rheumatic etiology) may also cause a headache.

The next most common type of headache, migraine, originates from the superficial arteries. It usually involves the superficial temporal arteries, but it can also involve the internal carotid arteries (Horton cephalalgia or cluster headaches), the occipital artery, and the intracranial arteries (e.g., hemiplegic migraine). Temporal arteritis and hypertension are two other important causes of headache originating from the extracranial arteries. The adjacent superficial nerves are a less common but important cause of headache. Occipital neuralgia may result from inflammation or compression of either the minor or major occipital nerve, and is often involved secondarily in muscle contraction headaches. This cause is established by blocking these two nerves (medially and laterally). Trigeminal neuralgia is no less important.

Moving to deeper layers, one encounters the skull, where osteomyelitis (e.g., tuberculous or syphilitic), primary and metastatic carcinomas, cranial stenosis, Paget disease, and skull fractures are important causes of headache. The temporomandibular joint (TMJ) is the origin of headache in the TMJ syndrome (usually caused by malocclusion) and RA. Important causes of headache affect the cervical spine. Cervical spondylosis is a major cause in elderly persons, but RA, spondylitis, spinal cord tumors, and metastatic disease of the vertebrae are also etiologies to consider.

Several common causes of headache come to mind when considering the organs of the head. Thus, the eyes are affected by refractive errors, astigmatism, and glaucoma, all etiologies of headache. The ear is affected by otitis media, mastoiditis, acoustic neuromas, and cholesteatomas. The nose is affected by infectious rhinitis, allergic rhinitis, Wegener granulomatosis, nicotine toxicity, fractures, and deviated septum, all causes of headache. Sinusitis (both the purulent and the vacuum type), sinus polyps, and tumors make checking the nasal sinuses important in analyzing the cause of headaches. Chronic sinusitis is almost never a cause of headache. Finally, the teeth should be investigated for caries, abscesses, and fillings that may be too close to the nerve root.

Intracranially there are very important but less common causes of headache. The meninges are the site of subarachnoid hemorrhages, subdural and epidural hematomas, meningitis,

and hydrocephalus. Missing one of these causes is a grave error. The cerebral arteries are the site of cerebral hemorrhages, thrombosis, and emboli, as well as aneurysms and arteriovenous anomalies. The cerebral veins, especially the venous sinuses, may become inflamed and thrombosed, producing a headache. The cranial nerves are the site of trigeminal neuralgia mentioned above and glossopharyngeal neuralgia.

Table 32 Headache—Extracranial and Cranial

Degenerative and Deficiency
Intoxication Idiopathic
Autoimmune Allergic
Skin   Herpes zoster
Abscess (scalp)
Muscle and Fascia         Muscle traction headache
Superficial Arteries Migraine       Migraine
Histamine cephalalgia
  Temporal arteritis    
Superficial Nerves   Occipital neuralgia     Trigeminal neuralgia
Sphenopalatine ganglion neuralgia
Skull   Tuberculosis
Metastatic carcinoma
Multiple myeloma
  Paget disease
Cranial stenosis
Hyperostosis frontalis
    Skull fracture Hyperparathyroidism
Temporomandibular joint         TMJ syndrome Malocclusion Rheumatoid arthritis    
Cervical Spine   Tuberculosis Cord tumor
Osteoarthritis Cervical spondylosis   Rheumatoid arthritis    
Sinuses   Sinusitis Sinus tumor or polyp   Vacuum sinus headache
Caffeine withdrawal
  Allergic sinusitis Fracture  
Eyes Retinal artery or vein occlusion Uveitis
Orbital tumor   Glaucoma
Refraction error
Orbital trauma
Corneal erosion
Ears   Otitis media
Acoustic neuroma
        Basilar fracture  
Teeth   Abscess   Dental caries       Irritation of nerve root by filling  
Nose Wegener granulomatosis Rhinitis
Schmincke tumor   Toxic rhinitis (e.g., nicotine) Deviated septum Allergic rhinitis Broken nose  

Table 33 Headache—Intracranial

Degenerative and Deficiency
Intoxication Idiopathic
Autoimmune Allergic
Meninges Subarachnoid hemorrhage Meningitis
Cystic hygroma
Epidural abscess
Rocky Mountain spotted fever
Hodgkin lymphoma
Other congenital disorders
  Subdural and epidural hematoma
Lumbar puncture headache
Cerebral Arteries Hemorrhage
A-V anomaly
Cerebral Veins   Venous sinus thrombosis           Subdural hematoma  
Cranial Nerves         Trigeminal and glossopharyngeal neuralgia   Optic neuritis    
Brain See above
Hypertensive encephalopathy
Encephalitis Parasite
Cerebral abscess
Primary and metastatic tumors   Benign intracranial hypertension
Other drugs
Postconcussion syndrome
Pituitary tumor
Systemic Disease Hypertension
Fever of any cause Leukemia
Hodgkin lymphoma
  Lead poisoning
Iodide toxicity
  Collagen disease   Diabetic acidosis
Menstrual tension
CHF, congestive heart failure; A-V, arteriovenous.

Although the brain itself is not tender, lesions of the brain cause increased intracranial pressure or traction on other painful structures, such as the intracranial arteries, venous sinuses, or nerves. A third of the cases of brain tumors present with a headache. Encephalitis produces a headache by the associated fever or meningeal irritation. Concussions, pituitary tumors, toxic encephalopathy from alcohol, bromides, and other substances are important causes, in addition to the cerebral hemorrhage, thrombosis, and emboli already mentioned. The various systemic diseases shown in Table 33 are too numerous to mention here, but fever of any etiology is an important cause and must not be forgotten, although this symptom is usually obvious.

Approach to the Diagnosis

The patient presenting with a history of headaches is an exciting diagnostic challenge. If one approaches the challenge simply on the basis of what is common, the patient most likely has migraine or muscle traction headache. But, wait a minute! Shouldn’t we look for serious conditions such as brain tumor, meningitis, or subarachnoid hemorrhage to avoid a serious mistake and a malpractice suit? First, check for nuchal rigidity to rule out meningitis and subarachnoid hemorrhage. Next, do a careful neurologic examination to rule out a brain tumor or other space-occupying lesion. These steps are particularly important in a patient who is experiencing his or her first serious headache. If there is nuchal rigidity or focal neurologic signs, it is wise to immediately refer the patient to a neurologist or neurosurgeon for further workup and possible hospitalization. The specialist will probably order a CT scan of the brain and follow that with a spinal tap if a subarachnoid hemorrhage or meningitis is suspected. It is clear that a CT scan should be done prior to a spinal tap if there are focal neurologic signs or papilledema. One other condition that must be considered in acute headache (particularly in elderly persons) is temporal arteritis. A sedimentation rate will usually be positive, but a neurology consult is axiomatic so that steroids can be started immediately.

In the patient with chronic or recurring headaches and no neurologic findings, it is wise to see the patient during the attack. Migraine headaches are typically associated with an aura or photophobia. Visual acuity should always be checked. Migraine and histamine headaches can be diagnosed by the response to sumatriptan by mouth or injection. If the headaches are due to chronic allergic or infectious rhinitis, relief can be had by spraying the turbinates with phenylephrine. Muscle traction headaches will often be relieved by occipital nerve blocks supporting the diagnosis. Compression of the superficial temporal artery will often relieve migraine temporarily supporting that diagnosis. Compression of the jugular veins will often give relief to patients with postspinal tap headaches.

If the patient is seen between headaches, certain prophylactic measures may help establish the diagnosis. For migraine, β-blockers may be prescribed; if the headaches are prevented, there is good support for the diagnosis. A course of corticosteroids may be initiated in patients with histamine (cluster) headaches to help establish the diagnosis. Muscle relaxants and/or tricyclic drugs may be given to help diagnose muscle contraction headaches.

The diagnostic workup of chronic headaches might include a CT scan of the brain, x-rays or CT scans of the sinuses, x-rays of the cervical spine, and routine blood work. Certainly if headache persists after careful follow-up, these need to be done. An ophthalmologist should be consulted to rule out astigmatism and glaucoma.

Other Useful Tests

  • Neurology consult

  • Sedimentation rate (temporal arteritis)

  • X-ray of the teeth (dental abscess)

  • MRI of the brain (brain tumor)

  • Spinal fluid analysis (meningitis, subarachnoid hemorrhage)

  • 24-hour blood pressure monitoring (pheochromocytoma)

  • 24-hour urine catecholamines (pheochromocytoma)

  • Tonometry (glaucoma)

  • MRI of the TMJs (TMJ syndrome)

  • Allergy skin tests (allergic rhinitis)

  • Temporal artery biopsy (temporal arteritis)

  • MR angiography (aneurysm)

Head Deformities

The best method to recall the causes of head deformities is to think of the mnemonic VINDICATE.

  • V—Vascular suggests Cooley anemia and the enlargement of head and cheekbones with a small bridge of the nose.

  • I—Infection recalls syphilis in which the head assumes the shape of a hot cross bun.


  • N—Neurologic disease includes microcephaly (small underdeveloped brain) and hydrocephaly (due to several causes); the most important diseases from a treatable standpoint are subdural hematomas, brain abscesses, and neoplasms. Cerebral palsy also should be included here.

  • D—Deficiency disease suggests rickets, in which the head is elongated, square, and flattened at the vertex.

  • I—Idiopathic disease recalls Paget disease. There is symmetric enlargement (occasionally a triangular shape) because the bones of the face do not enlarge. In facial hemiatrophy, one side of the head is smaller than the other.

  • C—Congenital disorders include scaphocephaly (elongated from front to back), oxycephaly or tower skull, hypertelorism (increased breadth of the skull and eyes far apart), mongolism, and brachycephaly.

  • A—Achondrodysplasia suggests a large head with a broad nose and prognathism.

  • T—Trauma recalls injury to the skull, causing edema (caput succedaneum), hematomas, and fractures.

  • E—Endocrine disorders such as acromegaly, myxedema, and cretinism cause a large head. Acromegaly is usually easily distinguishable by the protruding jaw.

Approach to the Diagnosis

Obviously, the most important thing in the workup of this symptom is a good neurologic examination and a skull x-ray film. Other studies will be dictated by the findings of the above. A blood count and morphology study will be worthwhile if Cooley anemia is suspected and Wassermann or fluorescent treponemal antibody absorption (FTA-ABS) test if congenital syphilis is suspected. Positional head deformity is most commonly caused by a child sleeping frequently in the supine position.

Other Useful Tests

  • Chemistry panel (rickets, Paget disease)

  • Serum 25-OHD and 1,25-(OH)2 D3 (vitamin D deficiency)

  • Sickle cell preparation (sickle cell anemia)

  • Bone scan (Paget disease)

  • Serum growth hormone level (acromegaly)

  • CT scan of brain (acromegaly, meningioma)

Head Mass

A localized mass on the head is usually a skin lesion, a lesion of the bone, or a protrusion of intracranial tissue through the bone. An extensive discussion of skin masses may be found on page 381, but most head masses originating from the skin are sebaceous cysts, carbuncles, or lipomas. Lesions of the skull that may present as focal lesions are metastatic tumors, multiple myeloma, osteitis fibrosa cystica (hyperparathyroidism), and osteomas. Brain tumors, subdural hematomas, and epidural abscesses may cause proliferation of the bone over the lesion and produce a mass. Congenital meningoceles and meningoencephaloceles may protrude through defects in the skull, producing large focal lesions in the midline.

Approach to the Diagnosis

The approach to the diagnosis includes excision or biopsy of skin lesions, skull x-rays, CT scans, bone scans, and, if necessary, a bone biopsy. A neurosurgeon should be consulted before ordering expensive diagnostic tests.


True heartburn (see also sections on indigestion, page 264 and anorexia, page 55) may be defined as a burning pain in the substernal area or midepigastrium, which is usually increased by swallowing and which is almost invariably due to esophagitis from gastric reflux. There are other causes, however, and the problem for the diagnostician is how best to recall these in the clinical situation. From an etiologic standpoint inflammation is almost invariably the culprit, although myocardial infarction or angina pectoris are two frequent causes that are not inflammatory.

Anatomically, the best approach is to move in a target-like fashion from the intrinsic portion of the esophagus and stomach peripherally. Thus, in the first zone, one encounters esophagitis, gastritis, and gastric ulcers. In the second zone, one encounters hiatal hernia (which, of course, predisposes to esophagitis), pericarditis, mediastinitis, and gastrojejunostomy complications. In the third zone, one visualizes cholecystitis (which probably induces a bile esophagitis), pancreatitis, myocardial infarction or coronary insufficiency, pleurisy, and intestinal obstruction. In the fourth zone, one recalls systemic diseases such as uremia, severe emphysema, cirrhosis, and congestive heart failure (CHF) (which probably causes gastritis or gastric ulcers).

Approach to the Diagnosis

The approach to the diagnosis of heartburn is similar to that of any GI complaint, but a few clinical tricks will help decide whether it is intrinsic or extrinsic, especially if the upper GI series is negative. Always order an esophagram. If the patient has the pain when in your office, administer a tablespoon or two of lidocaine (Xylocaine viscous). If the patient gets relief in 5 to 10 minutes, the heartburn is probably caused by esophagitis. Further confirmation can be obtained by a Bernstein test. In this test, solutions of normal saline and 0.10 normal HCl are administered by intravenous tubing into the lower esophagus, alternating one with the other. If the patient invariably experiences pain when the 0.10 normal HCl is administered, esophagitis is confirmed. Esophagoscopy and gastroscopy will reveal most intrinsic lesions with certainty, but occasionally they are normal in esophagitis. Manometric studies of the esophagus are the best way to diagnose esophageal reflux. If the episodes are frequent but relatively brief, a trial of nitroglycerin may diagnose angina pectoris. Coronary insufficiency may also be confirmed by an exercise tolerance test. Cholecystogram and liver and pancreatic function studies may also be indicated.

Other Useful Tests

  • Ambulatory pH monitoring (esophageal reflux)

  • Gallbladder sonogram (cholecystitis)

  • Thallium scan (coronary insufficiency)

  • Acid barium swallow (esophagitis)

  • Therapeutic trial of nitroglycerin (coronary insufficiency)

  • Holter monitoring (coronary insufficiency)

  • Coronary angiogram (coronary insufficiency)

  • Therapeutic trial of proton pump inhibitors (reflux esophagitis)

Hematemesis and Melena

Hematemesis means vomiting or regurgitation of frank bright red blood or coffee-ground material that is positive
for occult blood. It may be differentiated from hemoptysis because it usually gives an acidic reaction to Nitrazine paper. It may be swallowed blood from any site in the oral cavity or nasopharynx, thus careful examination of these areas must be done. Melena is the passage of black tarry stools.

Head deformities.

The differential diagnosis of hematemesis, like that for bleeding from other body orifices, is best developed with the use of anatomy. Thus, beginning with the esophagus and working down to the ligament of Treitz and at the same time cross-indexing each structure with the various etiologies, one can make a chart like Table 34.

The major causes are illustrated on pages 208 and 213. In the esophagus the most common causes are varices, reflux esophagitis, carcinoma, and the Mallory–Weiss syndrome. One should not forget foreign bodies or irritants
such as lye, especially in children. Barrett esophagitis and ulcers caused by ectopic gastric mucosa are rare congenital causes of hematemesis. Finally, aortic aneurysms, mediastinal tumors, and carcinomas of the lung may ulcerate through the esophagus and bleed.

Head mass.

In the stomach, inflammation, especially gastritis and ulcers, is a prominent cause. Aspirin or alcohol, however, is often the cause. Varices of the cardia of the stomach may bleed. Carcinomas and hereditary telangiectasia are less common causes. Duodenal ulcers are usually the cause of bleeding from the duodenum, but occasionally neoplasms and regional ileitis may be involved. Ulceration of gallstones through the gallbladder and duodenal wall is another rare cause of bleeding from this site. The pancreas is included in the drawing because occasionally one encounters gross hematemesis during acute hemorrhagic pancreatitis when blood pours out of the duct and is vomited. The most common cause of bleeding from the small intestine is angiodysplasia.

Trauma is an important cause of bleeding from all the aforementioned sites, especially following intubation or surgery. Blood dyscrasias associated with coagulation disorders should be looked for immediately whenever a focal cause of hematemesis cannot be found, especially if bleeding is massive.


Approach to the Diagnosis

When confronted with solid evidence of hematemesis, the clinician should not waste valuable time on a thorough history and physical examination when endoscopy is more important in both diagnosis and therapy. Ordering a type and cross for multiple units of blood, coagulation studies, and the other tests listed below should also be done immediately in most cases. History of alcoholism, use of aspirin and other drugs, and previous ulcers or esophageal disease is important to get while preparing for endoscopy and other emergency procedures. Patients without massive or recent acute hematemesis or melena may be approached with traditional methods. A history of vomiting nonhemorrhagic gastric fluid before the onset of hematemesis is helpful in diagnosing a Mallory–Weiss syndrome. Remember black stools can be caused by Pepto-Bismol, iron, spinach, or licorice ingestion.

Table 34 Hematemesis and Melena

Degenerative and Deficiency
Autoimmune Allergic
Esophagus Esophageal varices
Aortic aneurysm
Reflux esophagitis
Trypanosomiasis cruzi
Carcinomas of esophagus and lung   Lye and other irritants
Foreign body
Hiatal hernia
Scleroderma Foreign body
Nasogastric tube
Mallory–Weiss syndrome
Stomach Cardiac varices
Ruptured aneurysm
Gastric ulcer
Carcinoma Atrophic gastritis Alcoholic gastritis, aspirin, and other drugs (e.g., arsenic) Hereditary telangiectasia   Perforation and laceration surgery Zollinger–Ellison syndrome
Duodenum   Ulcer         Regional ileitis Perforation and laceration surgery Zollinger–Ellison syndrome
Pancreas   Acute pancreatitis (hemorrhagic)              
Blood     Leukemia
Aplastic anemia
Vitamin K deficiency
Other drugs
Hemophilia and other hereditary coagulation disorders ITP
Collagen disease and other causes of thrombocytopenia
ITP, idiopathic thrombocytopenic purpura.

Hematemesis and melena.

Other Useful Tests

  • Complete blood count (CBC) (anemia of blood loss)

  • Chemistry panel (liver disease, kidney disease)

  • Stool for occult blood or fecal immunochemical testing (FIT) (ulcer, neoplasm, diverticulitis)

  • Gastric analysis (ulcer, neoplasm)

  • Liver function tests (esophageal varices)

  • Upper GI series and esophagram (reflux esophagitis, ulcer, esophageal carcinoma, gastric carcinoma)

  • Coagulation studies (e.g., blood dyscrasias, hemophilia)

  • Barium enema (colon neoplasm, diverticulitis)

  • Small-bowel series (neoplasm, diverticulitis)

  • CT scan of abdomen (neoplasm)

  • Colonoscopy (colon neoplasm, bleeding diverticulum)

  • CT angiography or catheter arteriogram (mesenteric thrombosis)

  • Fluorescein dye string test (to determine site of occult bleeding)

  • Nuclear scan (to detect bleeding site)

  • Breath test and stool antigen for Helicobacter pylori (peptic ulcer)

  • Ultrasonography (esophageal varices)

  • Capsule endoscopy (bleeding sites in the small intestine)


Using the anatomic approach, the physician can arrive at most of the causes of hematuria (Table 35). One need only visualize the urinary tract and proceed from the kidney on down to get a differential list. Let us apply the mnemonic VINDICATE to the kidney.

  • V—Vascular diseases make one think of embolic glomerulonephritis, renal vein thrombosis, and subacute bacterial endocarditis (SBE).

  • I—Infectious causes of hematuria are pyelonephritis (infrequently) and renal TB.

  • N—Neoplasms that may present with hematuria are hypernephromas and papillomas and carcinomas of the renal pelvis. Wilms tumors present with hematuria less frequently.

  • D—Degenerative diseases rarely present with hematuria as in other organ systems.

  • I—Intoxicants such as sulfa drugs (that lead to nephrocalcinosis), mercury poisoning, and blood transfusion reactions are common causes of gross or microscopic hematuria.

  • C—Congenital lesions such as polycystic kidneys and medullary sponge kidneys cause hematuria and predispose to stones and infections that may present with hematuria.

  • A—Autoimmune conditions such as acute and chronic glomerulonephritis, Goodpasture disease, Wegener midline granulomatosis, and lupus erythematosus commonly present with hematuria.

  • T—Trauma to any organ causes hemorrhages, and the kidney is no exception. Hematuria after automobile or other accidents should signal the need for hospitalization, intravenous pyelogram (IVP), and close observation of vital signs. Hematuria may present with a crush injury to any muscle or a burn. Injury to muscle (rhabdomyolysis) may also cause a positive urine dipstick test for blood because of myoglobin released by the muscle.

  • E—Endocrine–metabolic diseases caused by stones. Most calcium stones are not caused by hyperparathyroidism, but it should always be considered a possibility. Urate stones are usually caused by gout, and cystine stones are always associated with congenital cystinuria.

    • Ureter: Stones, papillomas, and congenital defects (contributing to stones) are the most likely causes here.

    • Bladder: Vascular disease is infrequently a cause, but cystitis (especially acute or “honeymoon” type) is a common cause. Stones, neoplasms (papillomas and transitional cell carcinomas), and foreign bodies are the next most likely causes. Trauma should not be forgotten, especially because of the numerous instances of various instruments being introduced into the bladder.

    • Prostate: Neoplasms of the prostate occasionally cause hematuria, but most other etiologic conditions (prostatitis) are rarely associated with gross or microscopic hematuria.

    • Urethra: Stones, neoplasms, and infections of the urethra may all cause hematuria, but very infrequently.

Using biochemistry as the basic chemistry, do not forget the coagulation disorders that may cause hematuria. Thus hematuria is often found in idiopathic thrombocytopenia purpura and in almost any disorder in which the platelet count drops below 40,000 cells/mm2. Hemophiliacs may present with hematuria. Patients given too much warfarin (Coumadin) will often get hematuria. Fibrinolysins and afibrinogenemia will also cause hematuria.

From this exercise, it should be evident that arriving at the causes of hematuria is not difficult if one visualizes the anatomy of the urinary tree and then considers each etiologic category in this light.

Approach to the Diagnosis

The clinical picture will point to the diagnosis in many cases. If there is a history of abdominal trauma, a contusion or laceration of the kidney or bladder should be suspected. Massive trauma anywhere prompts a tentative diagnosis of crush syndrome. This will cause myoglobinuria as well as hematuria. Purpura or bleeding from other sites suggests a coagulation disorder. Severe colicky pain in the abdomen suggests kidney stone. A long history of hypertension suggests polycystic kidneys, renal artery stenosis, or glomerulonephritis. A history of fever and rheumatic valvular disease suggests SBE with renal embolism. Painless hematuria in an otherwise healthy-looking adult suggests neoplasm, whereas painful hematuria with frequency and dysuria suggests cystitis. Hematuria and a flank mass would make a neoplasm or polycystic kidney likely. Red cell casts in the sediment indicate the bleeding is coming from the kidney. No red cells in the presence of a positive dipstick test for blood indicates hemoglobinuria. Clots in the urine should suggest that the lesion is in the bladder.

The initial workup should include a CBC, urinalysis, urine culture, chemistry panel, flat plate of the abdomen to assess the presence of stones and kidney size, and personal examination of the urinary sediment. If a renal calculus is suspected, a noncontrast helical CT scan is ordered immediately, and an urologist consulted. A three-glass test will help to localize the site of the bleeding. If there is blood in the initial specimen only, the urethra is probably the site of bleeding. If the blood is primarily in the final specimen, the bladder is most likely the site of bleeding. Equal blood discoloration in all specimens points to a renal lesion.

If renal TB is suspected, an acid-fast bacillus (AFB) smear and culture is done. If collagen disease is suspected, an ANA analysis and anti–double-strand DNA antibody titer is ordered.

If a renal carcinoma is suspected, a CT scan of the abdomen is probably the best study to order, but the advice of an urologist ought to be sought. Ultrasonography is useful in differentiating cysts from tumors. If a bladder neoplasm is suspected, cystoscopy will be done. If renal artery embolism or thrombosis is suspected, renal angiography may need to be done to clearly make the diagnosis.

Other Useful Tests

  • Chest x-ray (TB, Goodpasture disease)

  • Tuberculin test (TB)

  • Strain urine for stones

  • Serum complement (acute glomerulonephritis, lupus)

  • Antistreptolysin O (ASO) titer (acute glomerulonephritis)

  • Addis count (glomerulonephritis)

  • Blood cultures (SBE)

  • Coagulation studies (hemophilia, collagen disease, allergic purpura)

  • Plasma haptoglobins (hemolytic anemias)

  • Coombs test (hemolytic anemias)

  • Platelet count (thrombocytopenic purpura)

  • Renal biopsy (chronic nephritis, neoplasm)

  • Surgical exploration

  • Urine for BTA or NMP22 (bladder CA)

  • Urine cytology (Fish test) also useful to rule out bladder CA.

Hematemesis and melena.


Table 35 Hematuria

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Sep 23, 2018 | Posted by in CRITICAL CARE | Comments Off on H
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