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Dermatology - Polymorphous light eruption (PMLE)
PMLE refers to a collection of diverse, unexplained, acquired, and recurring skin rashes that occur as a delayed response to exposure to UV radiation. Polymorphic light eruption (PMLE) is the prevailing form of photodermatitis, typically occurring in individuals during their third decade of life. Prevalence is higher among women compared to men, as well as among those with lighter skin. Actinic prurigo is a genetic condition found in American Indians in both North and South America.
Lesions manifest during the early spring and summer seasons, characterized by the presence of erythematous macules, papules, plaques, and vesicles. Nevertheless, in every case, the eruption consistently manifests as only one kind, most commonly papular or papulovesicular. PMLE often manifests shortly after exposure and persists for a duration of 7-10 days. Occasionally, towards the end of the summer, the eruptions cease to happen, indicating a process of solidification. The symptoms include pruritus (itching that may occur before the rash appears) and paresthesia (tingling sensation).
Abnormalities
The papular and papulovesicular forms are the most common. Plaques or urticarial plaques are far less frequent. The lesions have a color spectrum ranging from pink to red. The eruption often avoids locations that are regularly exposed (such as the face and neck) and is most commonly seen on the forearms, V area of the neck, arms, and chest. Lesions may also manifest on the face in the absence of prior sun exposure.
The diagnosis is established when there is a delayed commencement of eruption, distinctive morphology, histopathological findings that exclude lupus erythematosus, and a history of the eruption disappearing within a few days. For plaque-type polymorphous light eruption (PMLE), it is necessary to perform a biopsy and immunofluorescence investigations in order to exclude the possibility of lupus. Photo-testing involves the use of both UVB and UVA.
Test sites are regularly subjected to daily exposure of UVB and UVA radiation for a duration of 1 week to 10 days, with varying levels of UV dosage. Confirmation of the diagnosis is achieved when a PMLE-like eruption appears in the test locations of over 50% of patients. The eruption observed in the test site closely resembles the sort of Polymorphous Light Eruption (PMLE) observed in that specific patient.
Sunblocks, including high-strength UVAUVB sunscreens, may not always provide complete protection, but they should always be the initial choice. Administering systemic β-carotene at a dosage of 60 mg three times a day for a duration of 2 weeks before to exposure can potentially prevent eruptions. Similarly, using oral prednisone at a dosage of 20 mg per day, starting 2 days before exposure and continuing for 2 days during exposure, may also have a preventive effect. Administering 40 mg of intramuscular triamcinolone acetonide a few days before exposure will effectively suppress an eruption.
PMLE refers to a collection of diverse, unexplained, acquired, and recurring skin rashes that occur as a delayed response to exposure to UV radiation. Polymorphic light eruption (PMLE) is the prevailing form of photodermatitis, typically occurring in individuals during their third decade of life. Prevalence is higher among women compared to men, as well as among those with lighter skin. Actinic prurigo is a genetic condition found in American Indians in both North and South America.
Lesions manifest during the early spring and summer seasons, characterized by the presence of erythematous macules, papules, plaques, and vesicles. Nevertheless, in every case, the eruption consistently manifests as only one kind, most commonly papular or papulovesicular. PMLE often manifests shortly after exposure and persists for a duration of 7-10 days. Occasionally, towards the end of the summer, the eruptions cease to happen, indicating a process of solidification. The symptoms include pruritus (itching that may occur before the rash appears) and paresthesia (tingling sensation).
Abnormalities
The papular and papulovesicular forms are the most common. Plaques or urticarial plaques are far less frequent. The lesions have a color spectrum ranging from pink to red. The eruption often avoids locations that are regularly exposed (such as the face and neck) and is most commonly seen on the forearms, V area of the neck, arms, and chest. Lesions may also manifest on the face in the absence of prior sun exposure.
The diagnosis is established when there is a delayed commencement of eruption, distinctive morphology, histopathological findings that exclude lupus erythematosus, and a history of the eruption disappearing within a few days. For plaque-type polymorphous light eruption (PMLE), it is necessary to perform a biopsy and immunofluorescence investigations in order to exclude the possibility of lupus. Photo-testing involves the use of both UVB and UVA.
Test sites are regularly subjected to daily exposure of UVB and UVA radiation for a duration of 1 week to 10 days, with varying levels of UV dosage. Confirmation of the diagnosis is achieved when a PMLE-like eruption appears in the test locations of over 50% of patients. The eruption observed in the test site closely resembles the sort of Polymorphous Light Eruption (PMLE) observed in that specific patient.
Sunblocks, including high-strength UVAUVB sunscreens, may not always provide complete protection, but they should always be the initial choice. Administering systemic β-carotene at a dosage of 60 mg three times a day for a duration of 2 weeks before to exposure can potentially prevent eruptions. Similarly, using oral prednisone at a dosage of 20 mg per day, starting 2 days before exposure and continuing for 2 days during exposure, may also have a preventive effect. Administering 40 mg of intramuscular triamcinolone acetonide a few days before exposure will effectively suppress an eruption.
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Dermatology - Disseminated Intravascular Coagulation
Disseminated intravascular coagulation is a prevalent condition characterized by abnormal blood clotting that occurs throughout the blood arteries. This disorder is commonly linked to many clinical situations such as bacterial sepsis, obstetric difficulties, disseminated malignancy, or severe trauma.
The clinical manifestations of DIC can vary from mild and asymptomatic to severe and potentially fatal. The symptoms manifest gradually over a period of hours to days, characterized by fever, chills, tachycardia, and potentially indicators of shock. Hemorrhage can also occur from various cutaneous sites, such as surgical wounds, venipuncture, or catheter sites. Bleeding from the gums may also happen.
Infarction (purpura fulminans) or extensive ecchymoses arise with sharp, irregular (“geographic”) boundaries with deep purple to blue color and erythematous halo and may evolve to hemorrhagic bullae or blue to black gangrene. Frequently, there are several symmetrical lesions located on the outermost parts of the limbs, regions subjected to pressure, lips, ears, nose, or torso. Peripheral acrocyanosis can progress to gangrene in the hands, feet, and tip of the nose, leading to autoamputation.
The diagnosis is made based on clinical observations and verified through coagulation testing. Possible causes of significant cutaneous infarctions that need to be considered are necrosis resulting from the start of warfarin treatment, heparin necrosis, calciphylaxis, and atheroembolization.
Administer systemic antimicrobials to treat infections. To manage bleeding or thrombosis, administer heparin, pentoxifylline, and protein C concentrate, while also providing supportive care.
Disseminated intravascular coagulation is a prevalent condition characterized by abnormal blood clotting that occurs throughout the blood arteries. This disorder is commonly linked to many clinical situations such as bacterial sepsis, obstetric difficulties, disseminated malignancy, or severe trauma.
The clinical manifestations of DIC can vary from mild and asymptomatic to severe and potentially fatal. The symptoms manifest gradually over a period of hours to days, characterized by fever, chills, tachycardia, and potentially indicators of shock. Hemorrhage can also occur from various cutaneous sites, such as surgical wounds, venipuncture, or catheter sites. Bleeding from the gums may also happen.
Infarction (purpura fulminans) or extensive ecchymoses arise with sharp, irregular (“geographic”) boundaries with deep purple to blue color and erythematous halo and may evolve to hemorrhagic bullae or blue to black gangrene. Frequently, there are several symmetrical lesions located on the outermost parts of the limbs, regions subjected to pressure, lips, ears, nose, or torso. Peripheral acrocyanosis can progress to gangrene in the hands, feet, and tip of the nose, leading to autoamputation.
The diagnosis is made based on clinical observations and verified through coagulation testing. Possible causes of significant cutaneous infarctions that need to be considered are necrosis resulting from the start of warfarin treatment, heparin necrosis, calciphylaxis, and atheroembolization.
Administer systemic antimicrobials to treat infections. To manage bleeding or thrombosis, administer heparin, pentoxifylline, and protein C concentrate, while also providing supportive care.
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Dermatology - Lentigo maligna melanoma (LMM)
LMM, or lentigo maligna melanoma, is a melanoma subtype that is quite uncommon, affecting less than 5% of light-skinned individuals. It primarily affects older adults, with a median age of beginning at 65 years. LMM typically appears on the portions of the body that are most exposed to the sun, such as the face and forearms.
LMM initially manifests as lentigo maligna (LM), which is a flat neoplasm located inside the epidermis. It is important to note that LM is not a precursor but rather a developing lesion of melanoma. Papular and nodular lesions indicate a transition from radial to vertical growth, indicating an infiltration into the dermis.
The process of LMM gradually transitions from LM over a span of many years, occasionally lasting as long as two decades.
Dermatoheliosis is almost always present in the background.
The lesions in question are flat and uniform macules, ranging in size from 0.5 cm to 20 cm. They often have well-defined borders, although they may occasionally exhibit fuzzy or extremely uneven edges, frequently with a notch. These lesions often have a "geographic" appearance, resembling inlets and peninsulas. Initial lesions appear tan, but more developed lesions exhibit a brown and black (speckled) appearance. These mature lesions resemble irregular networks of black markings on a brown backdrop, lacking any shades of red or blue.
Lentigo maligna melanoma LMM is characterized by the presence of red, white, and blue patches, bumps, or lumps, similar to LM but with a varied appearance. Occasionally, LMM may lack pigmentation, have a skin-colored appearance, and exhibit patchy redness, requiring a biopsy for diagnosis.
The diagnosis is established through clinical examination using dermoscopy and subsequently confirmed through histological analysis. The differential diagnosis includes seborrheic keratosis, which can be distinguished by the presence of scaling upon excoriation, and solar lentigo, which lacks the same level of intensity or variation in brown, dark brown, and black colors as found in LM.
Administer imiquimod to address first lesions promptly. Remove advanced lesions by excising tissue down to the fascia, ensuring 1-cm margins beyond the apparent lesion or biopsy scar. However, if the eyelids or critical organs are affected, smaller margins can be used. Utilize a Woods light and dermoscopy to delineate the boundaries of the lesion. Perform a biopsy on the sentinel nodes if the lesion measures more than 1 millimeter in thickness. Utilize skin flaps or grafts to achieve closure and restoration. Following the complete eradication of all identifiable tumors, it is advisable to contemplate the use of additional therapy based on the stage of the disease.
LMM, or lentigo maligna melanoma, is a melanoma subtype that is quite uncommon, affecting less than 5% of light-skinned individuals. It primarily affects older adults, with a median age of beginning at 65 years. LMM typically appears on the portions of the body that are most exposed to the sun, such as the face and forearms.
LMM initially manifests as lentigo maligna (LM), which is a flat neoplasm located inside the epidermis. It is important to note that LM is not a precursor but rather a developing lesion of melanoma. Papular and nodular lesions indicate a transition from radial to vertical growth, indicating an infiltration into the dermis.
The process of LMM gradually transitions from LM over a span of many years, occasionally lasting as long as two decades.
Dermatoheliosis is almost always present in the background.
The lesions in question are flat and uniform macules, ranging in size from 0.5 cm to 20 cm. They often have well-defined borders, although they may occasionally exhibit fuzzy or extremely uneven edges, frequently with a notch. These lesions often have a "geographic" appearance, resembling inlets and peninsulas. Initial lesions appear tan, but more developed lesions exhibit a brown and black (speckled) appearance. These mature lesions resemble irregular networks of black markings on a brown backdrop, lacking any shades of red or blue.
Lentigo maligna melanoma LMM is characterized by the presence of red, white, and blue patches, bumps, or lumps, similar to LM but with a varied appearance. Occasionally, LMM may lack pigmentation, have a skin-colored appearance, and exhibit patchy redness, requiring a biopsy for diagnosis.
The diagnosis is established through clinical examination using dermoscopy and subsequently confirmed through histological analysis. The differential diagnosis includes seborrheic keratosis, which can be distinguished by the presence of scaling upon excoriation, and solar lentigo, which lacks the same level of intensity or variation in brown, dark brown, and black colors as found in LM.
Administer imiquimod to address first lesions promptly. Remove advanced lesions by excising tissue down to the fascia, ensuring 1-cm margins beyond the apparent lesion or biopsy scar. However, if the eyelids or critical organs are affected, smaller margins can be used. Utilize a Woods light and dermoscopy to delineate the boundaries of the lesion. Perform a biopsy on the sentinel nodes if the lesion measures more than 1 millimeter in thickness. Utilize skin flaps or grafts to achieve closure and restoration. Following the complete eradication of all identifiable tumors, it is advisable to contemplate the use of additional therapy based on the stage of the disease.
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Symptoms and Signs – Differential Diagnosis of Cloudy Urine
• Use of multivitamin supplements
• Urinary tract infection
• Pyuria
• Phosphaturia
• Lipiduria
• Hyperoxaluria
• Diet high in purine-rich foods
• Concentrated urine
• Chyluria
• Use of multivitamin supplements
• Urinary tract infection
• Pyuria
• Phosphaturia
• Lipiduria
• Hyperoxaluria
• Diet high in purine-rich foods
• Concentrated urine
• Chyluria
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Symptoms and Signs – Differential Diagnosis of Clubbing
• Celiac disease
• Chronic liver disease, cirrhosis (particularly biliary and juvenile)
• Chronic trauma (jackhammer operators, machine workers)
• Cyanotic congenital heart disease
• Cystic fibrosis
• Endocrine (Graves’ disease, hyperparathyroidism)
• Extrapulmonary infectious process (subacute bacterial endocarditis, intestinal TB, bacterial or amebic dysentery, arterial graft sepsis)
• Hereditary (pachydermoperiostitis)
• Idiopathic
• Inflammatory bowel disease (IBD)
• Other neoplasm (GI, liver, Hodgkin’s disease, thymus, osteogenic sarcoma)
• Pneumoconiosis
• Pulmonary arteriovenous (AV) malformations
• Pulmonary infectious process (empyema, abscess, bronchiectasis, TB, chronic pneumonitis)
• Pulmonary neoplasm (lung, pleura)
• Sarcoidosis
• Thyroid acropachy
• Celiac disease
• Chronic liver disease, cirrhosis (particularly biliary and juvenile)
• Chronic trauma (jackhammer operators, machine workers)
• Cyanotic congenital heart disease
• Cystic fibrosis
• Endocrine (Graves’ disease, hyperparathyroidism)
• Extrapulmonary infectious process (subacute bacterial endocarditis, intestinal TB, bacterial or amebic dysentery, arterial graft sepsis)
• Hereditary (pachydermoperiostitis)
• Idiopathic
• Inflammatory bowel disease (IBD)
• Other neoplasm (GI, liver, Hodgkin’s disease, thymus, osteogenic sarcoma)
• Pneumoconiosis
• Pulmonary arteriovenous (AV) malformations
• Pulmonary infectious process (empyema, abscess, bronchiectasis, TB, chronic pneumonitis)
• Pulmonary neoplasm (lung, pleura)
• Sarcoidosis
• Thyroid acropachy
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Symptoms and Signs – Differential Diagnosis of Cobalamin Deficiency
NUTRITIONAL COBALAMIN DEFICIENCY (I.E., INSUFFICIENT COBALAMIN INTAKE)
• Vegetarians, poverty-imposed near-vegetarians, breast-fed infants of mothers with pernicious anemia
ABNORMAL INTRAGASTRIC EVENTS (I.E., INADEQUATE
PROTEOLYSIS OF FOOD COBALAMIN)
• Atrophic gastritis, partial gastrectomy with hypochlorhydria, proton pump inhibitors, H2 blockers
LOSS OR ATROPHY OF GASTRIC OXYNTIC MUCOSA (I.E., DEFICIENT INTRINSIC FACTOR [IF] MOLECULES)
• Total or partial gastrectomy, pernicious anemia, caustic
destruction (lye)
ABNORMAL EVENTS IN SMALL BOWEL LUMEN
• Inadequate pancreatic protease (e.g., R-cobalamin not degraded, cobalamin not transferred to IF)
• Insufficient pancreatic protease (i.e., pancreatic insufficiency)
• Inactivation of pancreatic protease (i.e., Zollinger-Ellison syndrome)
• Usurping of luminal cobalamin (i.e., inadequate cobalamin binding to IF)
• By bacteria; during stasis syndromes (e.g., blind loops, pouches of diverticulosis, strictures, fistulas, anastomosis); impaired bowel motility (e.g., scleroderma); hypogammaglobulinemia
• By Diphyllobothrium latum (fish tapeworm)
DISORDERS OF ILEAL MUCOSA/IF-COBALAMIN RECEPTORS (I.E., IF-COBALAMIN NOT BOUND TO IFCOBALAMIN RECEPTORS)
• Diminished or absent IF-cobalamin receptors (e.g., ileal bypass, resection, fistula)
• Abnormal mucosal architecture/function (e.g., tropical or nontropical sprue, Crohn’s disease, tuberculous ileitis, infiltration by lymphomas, amyloidosis)
• IF/post IF–cobalamin receptor defects (e.g., Imerslund-Graesbeck syndrome, transcobalamin II [TC II] deficiency)
• Drug effects (e.g., Slow-K, metformin, cholestyramine, colchicine, neomycin)
DISORDERS OF PLASMA COBALAMIN TRANSPORT (I.E., TC II–COBALAMIN NOT DELIVERED TO TC II RECEPTORS)
• Congenital TC II deficiency, defective binding of TC II–cobalamin to TC II receptors (rare)
METABOLIC DISORDERS (I.E., COBALAMIN NOT USED BY CELLS)
• Inborn enzyme errors (rare)
• Acquired disorders (e.g., cobalamin functionally inactivated by irreversible oxidation, N2O inhalation)
NUTRITIONAL COBALAMIN DEFICIENCY (I.E., INSUFFICIENT COBALAMIN INTAKE)
• Vegetarians, poverty-imposed near-vegetarians, breast-fed infants of mothers with pernicious anemia
ABNORMAL INTRAGASTRIC EVENTS (I.E., INADEQUATE
PROTEOLYSIS OF FOOD COBALAMIN)
• Atrophic gastritis, partial gastrectomy with hypochlorhydria, proton pump inhibitors, H2 blockers
LOSS OR ATROPHY OF GASTRIC OXYNTIC MUCOSA (I.E., DEFICIENT INTRINSIC FACTOR [IF] MOLECULES)
• Total or partial gastrectomy, pernicious anemia, caustic
destruction (lye)
ABNORMAL EVENTS IN SMALL BOWEL LUMEN
• Inadequate pancreatic protease (e.g., R-cobalamin not degraded, cobalamin not transferred to IF)
• Insufficient pancreatic protease (i.e., pancreatic insufficiency)
• Inactivation of pancreatic protease (i.e., Zollinger-Ellison syndrome)
• Usurping of luminal cobalamin (i.e., inadequate cobalamin binding to IF)
• By bacteria; during stasis syndromes (e.g., blind loops, pouches of diverticulosis, strictures, fistulas, anastomosis); impaired bowel motility (e.g., scleroderma); hypogammaglobulinemia
• By Diphyllobothrium latum (fish tapeworm)
DISORDERS OF ILEAL MUCOSA/IF-COBALAMIN RECEPTORS (I.E., IF-COBALAMIN NOT BOUND TO IFCOBALAMIN RECEPTORS)
• Diminished or absent IF-cobalamin receptors (e.g., ileal bypass, resection, fistula)
• Abnormal mucosal architecture/function (e.g., tropical or nontropical sprue, Crohn’s disease, tuberculous ileitis, infiltration by lymphomas, amyloidosis)
• IF/post IF–cobalamin receptor defects (e.g., Imerslund-Graesbeck syndrome, transcobalamin II [TC II] deficiency)
• Drug effects (e.g., Slow-K, metformin, cholestyramine, colchicine, neomycin)
DISORDERS OF PLASMA COBALAMIN TRANSPORT (I.E., TC II–COBALAMIN NOT DELIVERED TO TC II RECEPTORS)
• Congenital TC II deficiency, defective binding of TC II–cobalamin to TC II receptors (rare)
METABOLIC DISORDERS (I.E., COBALAMIN NOT USED BY CELLS)
• Inborn enzyme errors (rare)
• Acquired disorders (e.g., cobalamin functionally inactivated by irreversible oxidation, N2O inhalation)
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Symptoms and Signs – Differential Diagnosis of Cocaine Overdose
• Methylenedioxyamphetamine (“ecstasy”) abuse
• Methamphetamine (“speed”) abuse
• Lysergic acid diethylamide (LSD) abuse
• Hyperthyroidism, panic disorder, pheochromocytoma
• Cathinone (“khat”) abuse
• Methylenedioxyamphetamine (“ecstasy”) abuse
• Methamphetamine (“speed”) abuse
• Lysergic acid diethylamide (LSD) abuse
• Hyperthyroidism, panic disorder, pheochromocytoma
• Cathinone (“khat”) abuse
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Symptoms and Signs – Differential Diagnosis of Coccidioidomycosis
• Acute pulmonary coccidioidomycoses: community-acquired pneumonias caused by Mycoplasma and Chlamydia; granulomatous diseases, such as Mycobacterium tuberculosis and sarcoidosis; other fungal diseases, such as Blastomyces dermatitidis and Histoplasma
capsulatum
• Coccidioidomas: true neoplasms
• Acute pulmonary coccidioidomycoses: community-acquired pneumonias caused by Mycoplasma and Chlamydia; granulomatous diseases, such as Mycobacterium tuberculosis and sarcoidosis; other fungal diseases, such as Blastomyces dermatitidis and Histoplasma
capsulatum
• Coccidioidomas: true neoplasms
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Symptoms and Signs – Differential Diagnosis of Acute Abdominal Colic
• Acute gastroenteritis
• Food poisoning
• Nonspecific causes, anxiety disorder
• Constipation
• Gastric outlet obstruction
• Chronic peptic ulceration
• Gastric cancer
SMALL BOWEL OBSTRUCTION
Adhesions
• Postsurgical
• Inflammatory (e.g., diverticular)
• Radiation
• Meckel’s diverticulum
• Metastatic
Stricture
• Ischemic
• Radiation
• Inflammatory (e.g., Crohn’s disease)
Volvulus
Intussusception
• Tumor (e.g., Peutz-Jeghers syndrome)
Superior Mesenteric Artery Syndrome
Intraluminal Bolus
• Gallstone
• Bezoar
Hernia
• Abdominal wall
• Internal
Neoplasm
• Benign (e.g., leiomyoma)
• Malignant (e.g., carcinoid tumor, adenocarcinoma)
• Large bowel obstruction
• Colon cancer
• Diverticular disease
• Volvulus
• Uterine
• Missed abortion
• Parturition
• Period pain
• Acute gastroenteritis
• Food poisoning
• Nonspecific causes, anxiety disorder
• Constipation
• Gastric outlet obstruction
• Chronic peptic ulceration
• Gastric cancer
SMALL BOWEL OBSTRUCTION
Adhesions
• Postsurgical
• Inflammatory (e.g., diverticular)
• Radiation
• Meckel’s diverticulum
• Metastatic
Stricture
• Ischemic
• Radiation
• Inflammatory (e.g., Crohn’s disease)
Volvulus
Intussusception
• Tumor (e.g., Peutz-Jeghers syndrome)
Superior Mesenteric Artery Syndrome
Intraluminal Bolus
• Gallstone
• Bezoar
Hernia
• Abdominal wall
• Internal
Neoplasm
• Benign (e.g., leiomyoma)
• Malignant (e.g., carcinoid tumor, adenocarcinoma)
• Large bowel obstruction
• Colon cancer
• Diverticular disease
• Volvulus
• Uterine
• Missed abortion
• Parturition
• Period pain
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Symptoms and Signs – Differential Diagnosis of Cutaneous Color Changes
BROWN
• Generalized: pituitary, adrenal, liver disease; adrenocorticotropic hormone (ACTH) producing tumor (e.g., oat cell lung carcinoma)
• Localized: nevi, neurofibromatosis
WHITE
• Generalized: albinism
• Localized: vitiligo, Raynaud’s syndrome
RED (ERYTHEMA)
• Generalized: fever, polycythemia, urticaria, viral exanthems
• Localized: inflammation, infection, Raynaud’s syndrome
YELLOW
• Generalized: liver disease, chronic renal disease, anemia
• Generalized (except sclera): hypothyroidism, increased intake of vegetables containing carotene
• Localized: resolving hematoma, infection, peripheral vascular insufficiency
BLUE
• Lips, mouth, nail beds: cardiovascular and pulmonary diseases, Raynaud’s syndrome
BROWN
• Generalized: pituitary, adrenal, liver disease; adrenocorticotropic hormone (ACTH) producing tumor (e.g., oat cell lung carcinoma)
• Localized: nevi, neurofibromatosis
WHITE
• Generalized: albinism
• Localized: vitiligo, Raynaud’s syndrome
RED (ERYTHEMA)
• Generalized: fever, polycythemia, urticaria, viral exanthems
• Localized: inflammation, infection, Raynaud’s syndrome
YELLOW
• Generalized: liver disease, chronic renal disease, anemia
• Generalized (except sclera): hypothyroidism, increased intake of vegetables containing carotene
• Localized: resolving hematoma, infection, peripheral vascular insufficiency
BLUE
• Lips, mouth, nail beds: cardiovascular and pulmonary diseases, Raynaud’s syndrome
