Nail Changes

There are various types of nail changes, such as thickening (onychogryposis), thinning, deformity, and separation from the nail bed (onycholysis). Whenever a peculiarity of the nail exists, the mnemonic VINDICATE will help to recall all the causes.

  • V—Vascular disease includes the anoxic disorders that cause clubbing (see page 97), iron deficiency anemia that causes spoon nails or koilonychia, Raynaud disease, vasculitis (periarteritis nodosa), and peripheral arteriosclerosis, which causes dystrophy or onychogryposis of the nails.

  • I—Inflammatory diseases that involve the nail bring to mind fungus infections causing onychia (nail bed inflammation), paronychia, syphilis (which can cause almost any nail change), subacute bacterial endocarditis (SBE), and trichinosis, which causes splinter hemorrhages of the nail.

  • N—Neoplasms do not usually cause nail changes, with the exception of clubbing and pallor from secondary anemia. Chondromas, melanomas, and angiomas are a few neoplasms that do. Intestinal polyposis may cause nail atrophy. The N, however, can be used to recall neurologic disorders such as peripheral neuropathy (dystrophy or onychogryposis), syringomyelia, and multiple sclerosis.

  • D—suggests deficiency diseases such as avitaminosis (B2 and D).

  • I—Intoxication includes arsenic (white lines and transverse ridges across the nails) and radiodermatitis.

  • C—Congenital disorders include psoriasis, congenital ectodermal defects, absence of nails (onychia), micronychia, and macronychia.

  • A—Autoimmune disorders suggest scleroderma, periarteritis nodosa, eczema, and lupus.

  • T—Trauma causes the familiar subungual hematoma that turns the nail to turn dark red or black.

  • E—Endocrine disorders are probably some of the most important causes of nail changes. Hypothyroidism produces nail dystrophy, brittleness, and onycholysis; similar changes, plus spooning of the nails, occur in hyperthyroidism. In hypopituitarism, these may be dystrophy, loss of the subcuticular moons, and spooning. Thickening and transverse grooving of the nails may be seen in hypoparathyroidism.

Approach to the Diagnosis

The diagnosis of nail abnormalities begins by correlating the nail changes with other findings (e.g., neurologic and endocrinologic). Laboratory workup depends on the particular disease or diseases suggested by the nail changes (see Appendix A).

Other Useful Tests

  • Complete blood count (CBC) (iron deficiency anemia)

  • Sedimentation rate (chronic infectious disease)

  • Blood cultures (SBE)

  • Trichinella antibody titer (trichinosis)

  • Free thyroxine (FT4) and sensitive thyroid-stimulating hormone levels (hyperthyroidism, hypothyroidism)

  • Serum parathyroid hormone (PTH) (hypoparathyroidism)

  • Serum growth hormone, luteinizing hormone, follicle-stimulating hormone (hypopituitarism)

  • Computed tomography (CT) scan of the brain (pituitary tumor)

  • Chest x-ray (neoplasm, tuberculosis, bronchiectasis)

  • Arterial blood gas (pulmonary disease, heart disease)

  • Hair analysis for arsenic (arsenic poisoning)

  • Antinuclear antibody (ANA) analysis (collagen disease)

  • Glucose tolerance test (diabetic arteriolar sclerosis)

Nasal Discharge

With nasal discharge (rhinorrhea and postnasal drip), anatomy is the key. In visualizing the structure from outside in, one encounters the external nares; the choana with the turbinates; the maxillary, ethmoid, frontal, and sphenoid sinuses; and the nasopharynx with the openings of the eustachian tubes surrounded by the adenoids. In addition, the inferior meatus provides the opening for the nasolacrimal ducts. The etiologies of a nonbloody discharge of the nose are almost invariably inflammatory (infectious or allergic), but a fracture of the sinuses or cribriform plate may cause a cerebrospinal fluid (CSF) rhinorrhea. As in nonbloody discharges elsewhere, it is incumbent on the diagnostician to keep the possibility of neoplasm, foreign body, and other causes of obstruction in mind, because these may set the stage for infection.

Nasal conditions causing acute nonbloody rhinorrhea include the common cold (due to any one of at least 60 viruses), viral influenza, pertussis, measles, and allergic rhinitis (hay fever). The discharge is at first clear; however, after a few hours of obstruction, secondary bacterial infection may set in and the discharge often becomes purulent. Chronic rhinitis is usually allergic, bacterial, or fungal (as in mucormycosis), but it can be on an autoimmune basis (Wegener granulomatosis). Toxins in the environment (e.g., smoke) may cause serous rhinorrhea. Too frequent use of nasal sprays and cocaine should always be considered. Chronic rhinitis may also be idiopathic (vasomotor rhinitis).

Nail changes.

The sinuses may be inflamed in the same conditions that involve the nose. However, concern about whether a discharge is coming from the sinuses arises when the discharge becomes purulent, when there is associated pain over the sinus, or when the discharge becomes chronic. In chronic sinusitis the discharge may frequently be a postnasal drip.

The nasopharynx is also involved by the same viral, bacterial, and fungal conditions as the rest of the nasal passages, but, in addition, diphtheria may begin here. If the adenoids become large enough, they may obstruct the nasal canals and produce a secondary bacterial rhinitis with discharge.

Nasal discharge.

Because the nasolacrimal ducts open into the inferior meatus, any eye condition that may cause excessive tearing may also produce rhinorrhea. The unilateral rhinorrhea of histamine headaches is partially related to this mechanism, as is trigeminal neuralgia.

Approach to the Diagnosis

The diagnosis of nonbloody rhinorrhea is not usually difficult in acute cases because it is frequently due to the common cold or allergic rhinitis (in which case the history will be helpful). However, the first thing to do is eliminate nasal sprays. When rhinorrhea persists, a smear for eosinophils and appropriate skin testing are useful if the discharge is nonpurulent; Gram stain, culture for bacteria and fungi, and x-rays of the sinuses will be valuable if the discharge is purulent. Cerebrospinal rhinorrhea is a possibility. This can now be confirmed by immunologic testing of the nasal discharge for β-2-transferrin. Idiopathic vasomotor rhinitis can be diagnosed by the response to Atrovent (topical anticholinergic agents). A CT scan is the preferred method to diagnose sinusitis.

Other Useful Tests

  • CBC (infection)

  • Sedimentation rate (infection)

  • Tuberculin test

  • Venereal disease research laboratory (VDRL) test

  • Fluorescent treponemal antibody absorption (FTA-ABS) test (more definitive test for syphilis)

  • ANA analysis (collagen disease)

  • Antineutrophil cytoplasmic antigen (ANCA) antibodies for Wegener granulomatosis

  • Fungal culture (mucormycosis)

  • Nasopharyngoscopy (neoplasm, granuloma)

  • CT scan of brain and sinuses (neoplasm, sinus abscess)

  • Biopsy

  • Radioimmunosorbent assay study of CSF (cerebrospinal rhinorrhea)

  • Viral antigen testing (influenza)

Nasal Mass or Swelling

Although anatomy may assist somewhat in developing the differential here, it is probably an unnecessary exercise because the mnemonic MINT will bring to mind virtually all the etiologies.

  • M—Malformation reminds one of the broad nose of cretinism, Down syndrome, gargoylism, myxedema, and acromegaly.

  • I—Inflammation suggests carbuncles; cellulitis; syphilis; acne rosacea with rhinophyma; Wegener midline granuloma; and granulomas from tuberculosis, aspergillosis, rhinosporidiosis, mucormycosis, and other chronic infections.

  • N—Neoplasms suggest carcinomas of the external nares, squamous cell carcinoma of the nasal mucosa (such as Schmincke tumors), and nasal polyps secondary to allergic rhinitis.

  • T—Trauma reminds one of fractures, dislocations, and contusions, although these diagnoses are usually obvious.

Approach to the Diagnosis

The diagnosis is not difficult except in the case of granulomas and carcinomas, when skillful biopsy and culture are necessary. In Wegener midline granuloma, a search for alveolitis and glomerulonephritis will help to determine the diagnosis. Serum for ANCA antibodies is often diagnostic.

Other Useful Tests

  • CBC (infection)

  • Nasal smear and culture

  • Tuberculin test (tuberculosis)

  • Acid-fast bacillus smear and culture (tuberculosis)

  • VDRL test (syphilis)

  • Fungal smear and culture (mucormycosis)

  • X-ray of skull and sinuses (granuloma, neoplasm)

  • CT scan of brain and sinuses (sinusitis, neoplasm, granuloma)

  • Nasal smear for eosinophils (nasal polyps)

  • Nasopharyngoscopy (polyps, carcinoma)

  • Serum immunoglobulin E (IgE) level (allergic rhinitis)

  • Radioallergosorbent test (RAST) (allergic rhinitis)

  • Allergy skin testing (nasal polyps)

Nasal Obstruction

The mnemonic MINTS will be very helpful in recalling the various causes of nasal obstruction.

  • M—Malformation prompts the recall of deviated nasal septum and congenital atresia.

  • I—Inflammation brings to mind nasal obstruction due to viral, bacterial, and allergic rhinitis and sinusitis. It should also help to recall the obstruction caused by mucormycosis in diabetes. Inflamed swollen adenoids cause acute and chronic obstruction.

  • N—Neoplasm reminds one of nasal polyps, fibromas, osteomas, teratomas, and advanced carcinomas.

  • T—Trauma prompts the recall of hematomas of the septum, fracture, and displacement of the nasal bones. T should also suggest toxic swelling of the membranes due to rhinitis medicamentosus.

  • S—Systemic causes facilitate the recall of Wegener granulomatosis.

Approach to the Diagnosis

If there is fever, one must suspect an upper respiratory infection or acute sinusitis and rhinitis. It is extremely important to ask about chronic use of topical nasal decongestants to rule out rhinitis medicamentosa. If allergic rhinitis is suspected, a nasal smear for eosinophils and serum IgE antibodies can be done. If there is a purulent discharge, smear and cultures for bacteria should be done. Wegener granulomatosis is diagnosed by an ANA, ANCA, or biopsy. In difficult cases, an otolaryngologist should be consulted.

Other Useful Tests

  • X-rays of the nose and sinuses (sinusitis, deviated septum, polyps)

  • CT scan of the sinuses (sinusitis, polyps)

  • Nasopharyngoscopy (adenoids, polyps, neoplasm)

  • Allergy skin tests (allergic rhinitis)

  • Viral antigen testing (influenza)

Nausea and Vomiting

These two should be considered together, because nausea is just a forme fruste of vomiting. A patient with acute nausea and vomiting and diarrhea almost always has viral or bacterial gastroenteritis although acute appendicitis, cholecystitis, and pancreatitis must be kept in mind. It is the chronic cases of nausea and vomiting that present a diagnostic dilemma. This symptom lends itself well to anatomic analysis, particularly by the target method illustrated on page 312. The focus should be on the gastrointestinal (GI) tract. Starting from the top and working to the bottom, and at the same time cross-indexing this with etiologies (Table 46), one can review the most important causes of vomiting.

In the nasopharynx, one encounters tonsillitis and foreign bodies. In the esophagus, achalasia, esophageal diverticulum, reflux esophagitis, and carcinoma are important,

although they are more likely to produce dysphagia (see page 128). In the stomach, gastritis, gastric ulcers, and gastric carcinoma are important causes of vomiting. A polyp, carcinoma, or ulcer at the pylorus is most likely to produce vomiting because of gastric outlet obstruction. In children, one must not forget pyloric stenosis. In the duodenum, one must consider not only ulcers and duodenitis but also the afferent loop obstructions that occur after Billroth II surgery and the “dumping syndrome” in Billroth I and II surgery. Bile gastritis is also a cause. Intestinal obstruction from a variety of causes (e.g., volvulus, intussusception, malrotation, bezoar, carcinoma, and regional ileitis) must
be considered in the jejunum and ileum. Parasites such as Strongyloides, Ascaris, and Taenia solium must also be considered in this part of the GI tract.

Table 46 Nausea and Vomiting

Degenerative and Deficiency
Congenital and Collagen
Autoimmune Allergic
Pharynx   Tonsillitis Diphtheria   Plummer-Vinson syndrome     Vincent angina Foreign body  
Esophagus Aortic aneurysm Esophagitis Chagas disease Carcinoma   Lye stricture Achalasia scleroderma   Foreign body  
Stomach   Gastritis Ulcers Carcinoma Pernicious Anemia Aspirin Reserpine Pyloric stenosis Cascade stomach     Gastrinoma Hyperparathyroidism
Duodenum   Ulcers
      Duodenal atresia or stenosis     Gastrinoma
Jejunum and Ileum Mesenteric thrombosis Tinea solium and other parasites (e.g., Salmonella, Shigella) Carcinoid Sarcoma Pellagra Malabsorption syndrome Botulism Whipple disease Meckel diverticulum Regional enteritis Ruptured viscus Vasoactive intestinal peptide syndrome
Appendix   Appendicitis Carcinoid         Rupture Fecalith  
Colon Mesenteric thrombosis Amebic colitis Staphylococcal colitis Carcinoma     Malrotation Diverticulum Ulcerative colitis Granulomatous colitis Ruptured viscus  
Gallbladder   Cholecystitis Cholangioma         Stone  
Pancreas   Pancreatitis Pancreatic cyst and carcinoma     Mucoviscidosis      
Kidneys Renal artery thrombosis Pyelonephritis Carcinoma with obstruction   Drug
Polycystic kidney Glomerulonephritis Rupture Stone
Pelvic Organs Torsion of ovary or cyst Pelvic inflammatory disease Ectopic pregnancy         Induced abortion  
Blood   Chronic anemia Leukemia Multiple myeloma Iron deficiency anemia Uremia        

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

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