Brief Manual of Primary Care Management

This is a recollection of various notes (some shamelessly lifted from internal use documents or various books over the years, some compiled and processed by myself) pertaining to possible courses of action towards certain medical pathologies presenting themselves spontaneously in a primary care setting.

The text assumes a limited degree of diagnostic autonomy and a higher dependence on other medical specialties, such as an ER room in a hospital or a sufficiently removed healthcare outpost instead of a usual doctor's office or a full-fledged multidisciplinary hospital. Clinical cases are therefore dictated by patient demand and are usually divided in two: benign yet clinically bothersome, or severe enough to merit admission to a hospital ward or ICU. Naturally, the intended scope of this article is towards physicians¹⁾.

As such, the role of the professional here is expected to be two-fold: not only one is expected to treat a patient (and, therefore, reach either an initial diagnosis or sieve the clinical presentation to narrow the scope of potential diagnoses), but also assume a competent logistic role to gauge sufficient criteria and answer when, how, where and how quickly to either approach nearby colleagues or use healthcare infrastructure services to continue treatment. The advantage of this is that the professional in this role is often limited to symptomatic treatment, but greatly limits the capacity for case follow-up and long-term treatment suggestions.

Defined by WHO as Stage III Hypertension: >180/XmmHg ∨ >X/110mmHg. Quickly evaluate associated conditions and conclude patient's risk level:

• Any hypertensive emergency where acute damage to target organs is either suspected or clinically defined (e.g. cardiac insufficiency, aortic dissection, hypertensive encephalopathy, acute myocardial ischemia…), or hypertension associated to another clinical emergency (e.g. stroke, acute renal insufficiency…) is to be considered high risk and requires priority management with imminent hospitalization if resolution isn't quickly achieved or careful posterior observation is required (in case of concomitant pathology, it's assumed that the pathology may be causing the hypertensive state or is otherwise in a feedback loop with it, and thus needs to be addressed first or simultaneously).
• Patients with a history of cardiovascular disease or anticoagulant medication, or patients with a clinical presentation mismatching typical hypertension symptomatology should be considered moderate risk and must be treated and observed accordingly.
• Isolated severe hypertension with typical symptoms and no evidence of target organ failure is low risk, usually well responsive to pharmacological treatment and warranting no more than posterior ambulatory control with Cardiology services.

Typical symptoms of severe hypertension include headache, neck pain, vertigo, nausea and vomiting, blurry vision, sometimes even dyspnea and chest pain.

Oral Route Pharmacology for Isolated Hypertension:

In ideal order, according to effectiveness and severity²⁾:

1. Enalapril 10-20mg
2. Amlodipin 5-10mg. Do not administer with previous or active bleeding.
3. Furosemide 40-120mg³⁾
4. Carvedilol 12.5-25mg.
5. You should ideally be able to solve the case without resorting to beta-blockers. The mere consideration of carvedilol should be considered treatment failure worthy of hospitalization.

Oral Route Pharmacology for Hypertensive Emergencies or Clinical Emergencies with Hypertension:

1. Most if not all of these require continuous infusion and are thus best suited for a hospital ward or the ICU.

• Confirmed or suspected stroke: With Stage III hypertension, wait 30 minutes and reevaluate. Do not treat if spontaneous reduction. If values remain at Stage III and anticoagulation/thrombolytic treatment is expected, administer Labetalol IV 10-20mg in 120 seconds followed by 20-40mg bolus every 10-20min until maximum of 300mg, repeatable every ~6-8h. Same if BP >220/XmmHg ∨ X/120-140mmHg. >X/140mmHg requires immediate and continuous Nitroprussiate management in ICU setting.
• Acute Renal Insufficiency: Dialysis + Labetalol 0.25-1mg/kg IV minibolus + Amlodipin 10mg. Hospitalization.

More often than not, chest pain “in front of the heart” responds to causes that have nothing to do with the cardiovascular system at all, such as muscle or osteoarticular pain; while these have little clinical relevance in an emergency context (Though they should never be ignored if they persist past an acceptable amount of time), some others such as pleuro-pulmonary pain and referred abdominal pain can be symptoms of incoming emergencies of a different etiology.

The differential diagnosis with utmost cardiovascular priority is that of acute miocardial infarction for reasons obvious to the reader, but some types of chest pain may also respond to equally ominous cases, such as compromise of major blood vessels or pericardium⁴⁾

AKA chest angina. Usually doesn't translate to cardiac ischemic injury, but the patient will remain terrified at the prospect that it might be. Constrictive/oppressive pain descriptions where the patient grasps at the center of his chest with a clawed hand, and irradiation to the left upper limb (or anywhere between the mandible and the navel!) warrants further study. Typical precordalgia responds well to rest (the usual trigger for such cardiovascular-originated chest pain is either effort or low oxygenation) and the administration of nitrites.

Typical precordialgia usually lasts no more than five minutes and thus only warrants outpatient cardiology consultation if symptoms cede, no previous history of cardiovascular disease exists, and no EKG alterations are present. Anything beyond 20 minutes should be enough to suspect a heart attack.

Atypical precordialgias (i.e. those that do not adhere to the description above) do not discard a cardiovascular origin outright, and also merit an EKG.

Any abnormality in the EKG is to be sent immediately to Intensive Care while laboratory results for cardiac enzymes (CPK, CPK-MB, Troponin) are processed.

A normal EKG with persistence of pain does not discard a coronary ischemic event: request cardiac enzymes (see above). Administer 300mg Aspirin, Clopidogrel 75mg, Atorvastatin 40mg (all orally) and await further results. Any enzyme indication of heart injury is enough to suspect indeterminate ischemic injury and warrants immediate Intensive Care derivation.

If breathing makes the pain worse, suspect pericarditis (check for pain reduction by instructing the patient to adopt a “Muslim prayer” posture). Sudden, excruciating pain with lack of peripheral pulse and progresive cognitive failure may be suggestive of aortic dissection.

The first line of treatment is continuous infusion of sodium nitroprussiate, which should be done at the Intensive Care/Coronary Unit level.

Too long a topic to properly cover here… perhaps in another article. On symptomatic arrhythmia, immediately begin with anticoagulant therapy (e.g. Enoxaparin 8kUI/24h) in an inpatient setting. Evaluate treatment urgency with Intensive Care and cardiology. Usually, this warrants the installation of a pacemaker which depends entirely on the institution's capabilities.

In a Primary Care setting, cases of cardiac insufficiency and general cases of ventricular dysfunction present themselves either as debut cases or as an acute exacerbation of a diagnosed case. Therefore, it becomes of utmost importance to evaluate four distinct diagnostic axes: Syndromic, Physiopathologic, Etiological and Functional.

The Syndromic diagnosis usually demands a confirmed diagnosis of cardiac insufficiency, for which cardiac ultrasonography is the gold standard and essentially mandatory in all cardiology literature; however, this may not a service usually found in a primary care setting and forces the practictioner to rely on stricter semiologic guidelines. The most valuable tools then become anamnesis, observation of pshyical findings, EKG, thoracic X-Ray and blood/urine analyses. Because these do not necessarily translate to life-threatening symptoms, they're as valid for a non-urgent diagnosis of cardiac insufficiency as for the immediate evaluation of symptomatic exacerbation.

Semiologic findings⁵⁾

“Left ventricle” cardiac insufficiency will present itself with dyspnea, coughing, fatigue; alongside bibasal “wet” crepitations on auscultation of the lungs (which indicate alveolar edema).

“Right ventricle” insufficiency has a more venous symptomatology and usually presents itself with congestion of neck veins⁶⁾, venous hypertension (once possible causes of hypervolemia or elevated cardiac workload are excluded, alongside other venous pathologies such as obstruction of the vena cava or evem an acute aorto-cava fistula secondary to an abdominal aneurysm rupture⁷⁾), hepatic congestion (hepatomegalia and its physical/laboratory semiology) and peripheral edema (which will first manifest in areas where gravity pools fluid, e.g. maleoli and sacrum in vertical and horizontal positions respectively, and evolve to a generalized edema with bilateral pulmonary edema, ascitis or even anasarca).

Ventricular dysfunction, or at the very least the underlying cardiopathy, tends to manifest with cardiomegaly (cardiothoracic index >0.5, apex beyond fifth left intercostal space) and cardiac gallop rhythm with persistent tachycardia (which indicates systolic failure). Atrial gallop (aka R4) without cardiomegaly suggests diastolic failure.

Radiographic findings

Beyond the rather self-evident finding of cardiomegaly which indicates systolic dysfunction (or its absence, which indicates diastolic dysfunction) and enlargement of the left atrium (which indicates biventricular failure), chest X-rays (of anteroposterior and latero-lateral projections) can indeed show signs of pulmonary hypertension with a confident degree of objectivity, though these require a well-trained eye to spot them. These are vascular redistribution (by congestion of the upper pulmonary veins), intersticial edema (by Kerley lines, edema within lung fissures, pleural effusion…), and alveolar edema.

EKG findings: Signs of enlarged cavities, heart blocks or full-blown arryhtmias, necrotic Q wave, etc. are commonplace. A perfectly normal, healthy EKG is enough to reconsider the diagnosis.

Laboratory findings:

• Anemia: Hb <5g% ∨ Hematocrit <25% will either cause or exacerbate dyspnea.
• Urea, Creatinin: Renal insufficiency alongside hypervolemia and cardiac volume overload will cause most if not all of the symptomatology of cardiac insufficiency⁸⁾.
• Proteinuria, glycosuria: Indicators of renal failure, which can be conducive to cardiac insufficiency or worsening it.
• Ionogram: Hyponatremia or K+ abnormalities are common complications.

Provisional diagnostic criteria⁹⁾:

• History of dyspnea, fatigue and/or malleolar edema either at rest or under physical stress
• Signs of venous pulmonary hypertension
• Bibasal pulmonary rattle in more than one third¹⁰⁾ of the auscultation area, or radiographical findings suggestive of venous pulmonary congestion
• Signs of systemic venous hypertension
• Enlarged neck veins
• Objective malleolar edema
• In systolic insufficiency: cardiomegaly, R3 heart gallop with persistent tachycardia
• In diastolic insufficiency: R4 gallop or prominent a-type venous waveform without cardiomegaly
• Diagnosis reinforced by exclusion of other possible causes of dyspnea, fatigue or edema.

Again, a definitive diagnosis can only be done with a cardiac ultrasound, but in primary or urgent care it's crucial to evaluate necessity of immediate treatment.

Therapeutic targets:

The main cardiologic issues that must be tackled during an episode of cardiac insufficiency include the treatment of symptoms first and then comes a mandatory followup (either ambulatory or inpatient) to avoid progression of the disease. This text focuses on the former.

The pharmacologic target consists of eliminating edema and reducing pre/afterload while increasing contractility. With this, a triple cocktail is suggested:

1. ACE Inhibitors: e.g. Enalapril 20mg orally. It's likely (and, in fact, recommended except when indicated otherwise) that the patient will be taking this dosage daily as it works very good for reducing mortality. ARBs can be used if ACE Inhibitors are contraindicated or unavailable. Second generation calcium inhibitors such as Amlodipin may or may not work in a pinch in non-ischemic insufficiencies.
2. Diuretics: Furosemide works good for this, and is adjusted empirically until congestive symptoms go away. Minimum amount necessary (a single 20ml ampoule at the beginning, for example) and removed once patient stabilizes.
3. Digoxin: 0.25g.

If BP is stable and no obvious contraindications are present, a beta-blocker such as carvedilol can be administered. This is usually not the case in an urgent care setting where the patient is clinically unstable. There's other medication for long-term treatment but that should be talked about once the patient is not actively dying.

Any chest pain of recent apparition (within 3 months), progressive (sudden worsening after a diagnosis of stable angina) or after a cardiac episode (say, within the first month of a heart attack) is considered to be an unstable angina and at high risk of developing an acute coronary syndrome, if not having one at the moment of presentation.

EKGs are essentially free so perform one. If there is no EKG anywhere near quit your job immediately. Very broadly, they can be normal, with negative T wave, with ST segment below baseline, or with ST segment above baseline. The first three are characteristic of acute coronary syndrome without ST elevation, and the latter… well, it's self-explanatory. If there's ST elevation then it's a proper heart attack and is to be sent to the ICU. ST below baseline usually carries a slightly negative prognosis and the negative T wave doesn't really mean much.

Any EKG that looks even mildly unclear should be corroborated with a cardiac enzyme tests for Troponin, CPK and CPK-MB; anything that looks like a definite heart attack should also be corroborated with cardiac enzyme tests. Therefore, always ask for cardiac enzyme tests when in doubt, even if it only usually gives out definitive results after six hours.

Immediately administer 300mg aspirin, isosorbide dinitrate 5mg (repeat every 5 minutes if needed, maximum 15mg), clopidogrel 300mg - all orally (isosorbide dinitrate will be most likely available sublingually). Administer oxygen if SatO2 is below 90. Analgesia can be managed by diluting 2-4mg of morphine in 10cc of saline and administering 2-8cc intravenously, which can be repeated every 5 to 15 minutes.

DO NOT administer isosorbide dinitrate if systolic BP <90mmHg!! DO NOT administer isosorbide dinitrate if there's a report or suspicion of consumption of sildenafil/taladafil/etc up to 48 hours prior!!

Once diagnosis has been reached the patient should be transfered to intensive care/coronary unit/anything more complex than your post to evaluate fibrinolytic treatment (anticoagulants and streptokinase) and vasodilation (usually in the form of nitroglicerin via infusion pump).

Recommended target time between the patient arriving and the patient getting fibrinolytic treatment (so-called “door-to-needle” time) is <30 minutes, or angioplasty (“door-to-balloon” time) <90 minutes. Depending on where you're at you'll probably not reach this time at all. Streptokinase is usually administered in a single 1.5MUI dosis diluted in 250cc saline over the course of sixty minutes, but if you find yourself administering streptokinase anywhere outside an ICU you're likely out of your depth.

Acute or chronic, it has a very characteristic pain (retrosternal, oppresive, which worsens with coughing and deglution and somewhat improves in a sitting position) and its pathognomonic sign is the presence of pericardial rub on auscultation.

EKG begins showing a diffuse, concave elevated ST segments with positive T waves on some derivations, which will evolve into a slow inversion of the T wave and a return to baseline of the ST segment before normalization (weeks or months later).

Presence of dyspnea, jugular distension, BP reduction during inspiration, tachychardia and tachypnea is indication of a pericardial effusion and, eventually, cardiac tamponade.

Evaluate need of pericardiocentesis. Admit patient, administer 500mg aspirin every 6 hours as long as pain and fever persist; stop administration gradually; add 500mg paracetamol every 6 hours if response is absent or insufficient.

If tuberculosis etiology is confirmed, coordinate with infectology services for long-term treatment (Isoniacide 300mg/d for six months + Rifampicin 600mg/d for six months + Pyrazinamide 30mg/kg/d for two months). If due to an acute bacterial infection, initiate strong antibiotic treatment and prepare patient for eventual surgical drainage.

“Intravascular bacterial infection of cardiovascular structures, including but not limited to endarteritis of major intrathoracic blood vessels and implanted intracardiac devices”.

Diagnosed by its classic medical semiology, strong anamnesis and confirmed with blood analysis for bacterial growth. It's usually good practice to get a transesophageal ultrasound done on symptomatic patients with artificial heart valves. Check the DUKE diagnostic criteria.

Most etiological agents behind endocarditis respond well to Penicillin (some may require cephalosporins or vancomicin instead), but duration and dosage is dependent on body weight and minimal inhibitory concentration. Get an infectologist.

Every patient with dyspnea or tachypnea ought to be promptly evaluated and look at previous Hx of cardiac insufficiency, hemorrhagic stroke, heart attack, trauma, sepsis… in short, it's the cardinal symptom of many etiologies that culminate in respiratory distress and insufficiency.

Infections will also be a common cause of dyspnea. At the time of this writing, a major cause of it is infection by SARS-COV-2¹¹⁾.

In a chest X-ray, evaluate for cardiomegaly and venous redistribution (or even intersticial edema with blurring of hilum, or alveolar edema). Jugular ingurgitation, heart gallop, precordalgia, EKG alterations, etc. are signs of acute cardiac insufficiency and treatment must begin immediately.

If no improvement is measured within six hours, respiratory frequency goes above 30/min, and diuresis diminishes to 40ml/h, immediate transfer to ICU is recommended - even more so if skin becomes cold and clammy and cognitive functions begin to decline. Sometimes even lividities are found.

If none of these elements are found or are otherwise impossible to evaluate, O2Sat of <94% is a good guideline for admission.

If sufficiently severe (based on symptoms and/or chest X-ray or CT scan showing significantly compromised pulmonary parenchyma) admit, blood culture x2, general laboratory blood tests.

• <60y, no comorbidities: Amoxicillin 500mg/8h orally for no less than 5 days, with no fever for 48h and O2Sat >94%

• >60y OR with comorbidities: Amoxicillin/Clavulanic 875/125mg /12h orally for no less than 5 days, with no fever for 48h and O2Sat >94%

• Patient in ward/on his way to ward: Ampicillin/Sulbactam 1.5g /6h EV. Same as above.

Patients allergic to beta-lactamics should be instead given Levofloxacin 750mg/d IV.

When in doubt, Xray. If doubt persists, CT.

Either non-massive (<200ml in 24h), massive (>200ml in 24h), or exsanguinating (>150ml/h or >1000ml/24h). If bleeding is minimal, stable, or has otherwise stopped, it can likely be dealt with in an outpatient setting; otherwise, or when in doubt, admit into ward.

Request completeblood work, coagulation tests, hepatic enzymes, urea, rheumatic testing (if available) and urinalysis. Arterial blood gases, Xrays or tomography, PPD…

Keep the airway open and well oxygenated. If coughing is too severe, it can be suppressed with codeine or, in a hurry, 10ml of a 2 ampoules moprhine:100ml saline solution administered orally. Keep head rest at 45º and begin correction of alterations in blood coagulation if so needed.

Semiologically well-defined; can be confirmed with a chest Xray both standing and in lateral decubitus or even more directly with a chest CT. Thoracentesis - if effusion is purulent or bloody, negotiate installation of K-227 drainage while admitting patient. All patients with pleural effusion should be sent to the ward for at least 24h evaluation.

Light criteria: pH < 7, pleural glycemia/plasma glycemia < 0.5, LDH > 1 kIU. Signs and symptoms similar to pleural effusion + bacterial infection. Chest xray usually helps.

Either spontaneous or traumatic, simple (rupture of subpleural bullae) or symptomatic (as part of an underlying pathology). Easily seen with a chest Xray and essentially confirmed with a chest CT.

If it has not gone beyond the mid-clavicular line (i.e. Grade I pneumothorax) one can keep the patient in observation for a while to see if there's spontaneous reexpansion of the affected lung. If it doesn't, or if it goes beyond the mid-clavicular line, drain by chest tube.

Considered solved if lung expansion is confirmed and air does no longer flow through the tube outwards. Any other case may require observation, bronchoscopy or direct surgical resolution.

Most frequent pulmonary pathology within the context of thoracic trauma. Small quantities can be syringed out, but larger quantities require a chest drain. >200ml/hr of drainage through chest tube within the first four-five hours or >500ml in an hour suggests a surgical approach. Replace lost blood if needed.

Pulmonary embolisms can become quickly lethal if treated late. Even then, one every ten cases of PE will be lethal. It can go from simple anxiety and tachypnea to sudden shock. Signs (tachypnea, rustling at auscultation, tachycardia, edema…), symptoms (dyspnea, pleural pain, untractacble anxiety, sometimes coughing…), radiological findings (Westermark, enlarged cardiac silhouette, Hampton sign, homolateral diaphragmatic elevation…), EKG findings (most notably T wave inversion @ DIII-aVF or V1-V4) are important, but mostly severely inespecific - clinical suspicion often comes from present risk factors instead, making initial diagnosis at the ER difficult if interrogation becomes difficult.

Acid-base analyses and arterial blood gases are useful as they usually show a prolonged condition of both hypoxemia and hypocapnia within a likely context of respiratory alkalosis.

Confirm diagnosis with D-Dimer test; any patient that shows up sufficiently messed up for a DDx of PE vs pulmonary edema vs asthma attack should get one.

Pulmonary angiographies, scintillographies are used to confirm the diagnosis but are likely to be beyond the scope of not just the ER, but also the entire institution.

Administer O2 and painkillers (ideally, NSAIDs). Signs of acute cardiac failure should be replied to with IV fluid and dopamine/dobutamine. Anticoagulate with Heparin: 5kIU IV bolus, then 1k every hour until aPTT values double. Switch to oral Heparine after 24hs.

Fibrinolytic treatment may also be required if eventual studies show abnormalities. This is, or should be, strictly ICU territory.

Not many specific signs and symptoms (see PE above), other than perhaps the classical pink foamy spit and profuse cold sweating. Administer oxygen until saturation at least above 90%. Morphine helps with pain, anxiety and will in fact dilate pulmonary vessels. Treat symptomatically afterwards, starting with 20mg furosemide IV. Anything beyond this requires continuous nitroglycerin administration which means ICU treatment.

Immediate goals are to ensure a clear airway with total cervical spine control and to ensure proper oxygenation and circulation. Severe thoracic lesions, and eventually other areas of trauma, should be at least stabilized and corrected. Peform every imaging study available, EKG and blood work including arterial blood gases. Trauma that cannot be immediately resolved within first examination will likely need surgical correction and patient should be admitted accordingly, though urgent decompression through chest tube drainage or centesis can be performed if needed. An open pneumothorax can (and should) be covered with a large enough piece of gauze drenched in vaseline and taped to the wound in three of its four sides to form a makeshift one-way valve and prevent the evolution into hypertensive pneumothorax until the operating room is ready.

Admit into ward if patient has cardiac entities (insufficiency, arryhtmias…), COPD is severe enough, dyspnea is too great, cyanotic presentation or is otherwise old. Otherwise, attempt stabilization with salbutamol every 20 minutes; add hydrocortisone 500mg IV if it persists. Admit if unresponsive to treatment.

Treatment guideline is essentially similar to COPD exacerbation (see above). Administer oxygen, evaluate resolution clinically if spirometry isn't available on hand.

Defined as anything distal to the duodenojejunal junction. Evaluate whether or not it's continuous, and whether the patient is hemodynamically stable. This defines whether a colonoscopy can be done later as an outpatient or immediately.

Eyeball whether or not rehydration and electrolyte replacement can be performed as an outpatient or immediately, combining both matters of professional convenience and toxemic potential (i.e. presence of bleeding, dehydration, duration of diarrhea). Loperamide 2-4mg on every bowel movement should be sufficient as primary care prescription; empiric antibiotic treatment can be started if there's signs of bacterial infection.

Immediate endoscopy should be performed if there's signs of suspicious weight loss, repeated vomiting, digestive hemorrhage, unexplained anemia, dysphagia, history of previous gastric ulcers, and so on. Otherwise, omeprazole 20mg/day or ranitidine 300mg/day for four weeks while avoiding tobacco, coffee and alcohol.

Request eventual endoscopy and GI outpatient consultation on suspicion of ulcer (pain 1-3 hours after eating, burping, bloating, even melena). Outpatient treatment is omeprazole 20mg/12h for 4-8 weeks + Amoxicilin 1g/12h for 1 week + Claritromicin 500mg/12h OR metronidazol 250mg/12h for 1 week. Stay alert for presentation of complications (hemorrhage, perforation, etc) within first visit.

98% of all cases of cholecystitis are associated to cholelithiasis. Presentation is as per usual but usually lacking good repsonse to OTC analgesics and with high WBC and bilirubin (mostly direct bilirubin); some may show up an increase of transaminase, ALF, or even amilase values. Request ultrasound if possible; admit immediately and begin antibiotic/strong analgesic treatment to de-escalate severity of symptoms. Surgical evaluation should follow soon.

Frank elevation of bilirubin and ALF will be the biggest indicators. Severe forms may even have CNS impairment and shock. DDx Acute Cholecystitis, jaundice is much more frequent and feverish symptoms much more pronounced in cholangitis. Admit with antibiotic and analgesic treatment, with strict hemodynamic and urinary control to catch systemic manifestations on time. Surgical procedure is indicated if case does not improve within 24-48 hours.

Aside from clinical signs, diagnosis can be confirmed by amilase/lipase serum blood levels (3x increase). Signs of organ failure are indication of ICU admission, otherwise send to general ward with analgesia, IV ranitidine and strict oral fast. Do not start with antibiotics unless severe or if other infectious foci are ascertained.

Profound anamnesis is vital: ask for a record of previous pathologies, surgeries, trauma, pharmacologic abuse… very noticeable abdominal muscle contraction. Percusion may yield loss of liver's characteristic timbre.

Central IV line, vesical catheter, nasogastric tube (for abdominal decompression). Start wide-spectrum antibiotic therapy.

Standing abdomen Xray first, look for infradiaphragmatic air. Immediate derivation to Surgery.

Abdominal pain is the cornerstone for proper diagnosis - mainly that which is spontaneous and exacerbates with respiratory movements. They usually begin as a vague epigastric pain that eventually localizes itself towards the territory of the affected organ (it remains vague, however, in generalized peritonitis). Evaluate pain at compression/decompression, abdominal wall contraction and tumefactions during palpation; exaggerated, localized noise increase at auscultation suggest peristaltic struggle against an obstacle.

Abdominal Xrays can show peritonitis, while ultrasound is good for biliary etiologies. When in doubt, CT. Always perform bloodwork in search of hepatopancreatic alterations and white blood cell count (get a coagulogram while you're at it, in case the surgical team decides the patient must go under the knife).

Specific treatment varies according to etiology.

Sudden pain in right iliac fossa. Most frequent (and most urgent) cause is acute appendicitis.

Lab results usually show WBC count of >10k/mm3. Ultrasound is good for diagnostic confirmation, or at least the confirmation of DDx (be sure to exclude gynecologic etiologies); CT may be overkill but it allows to measure appendix size, etc. IV fluids, pain control (but not too much so as to not hide signs and symptoms when reevaluated). Surgical team usually indicates antibiotics before the procedure.

Place a nasogastric tube and see what comes out of it: copious bilious extraction suggests high jejunal blockage while fecaloid matter in small quantities imply either a colonic or ileal obstruction. Standing abdominal Xrays (coin pile sign, etc).

Most of the treatment is done within the ward, surgically or otherwise; initial treatment is prokinetic medication, total digestive rest and enemas if so needed.

Painful, reddened tumefaction in the inguinal region alongside nausea, vomiting, abdominal distension, inability to pass gas… onset usually usdden.

If there are signs of strangulation never attempt to reduce it - don't shove a potentially necrotic piece of viscera back into the peritoneal cavity. This goes straight to surgery.

Either by obstruction or by massive intestinal vasoconstriction. There aren't much clinical signs other than a notable increase in WBC count once the necrotic territory begins to increase. Angiography is the ideal study (others are too inespecific aside from perhaps doppler ultrasound).

Usually requires ICU admission: central IV line, heparin IV bolus, maybe even a Swan-Ganz catheter…

Angiography is invaluable here; otherwise try to infer it based on its brutal clinical presentation and lab results (high WBC count, metabolic acidosis, high ALF and amilase); other imaging studies may be subsequently useful. Quickly rehidrate and begin antibiotic treatment until surgical team takes over - arterial ischemia has up to a 90% mortality rate.

Telltale sign is a case of hypovolemia that does not revert with adequate fluid/blood therapy (though it might get the patient out of shock), suggesting the presence of a large enough torn blood vessel. Clinically is, in short, a case of acute anemia with some abdominal pain.

Ultrasound is very useful here to ascertain the presence of liquid within the abdominal cavity. Everything else is surgical in nature.

Hemorrhoid surgery should be considered only after medical treatment because it's more often than not more problem than what it's worth. Treatment should instead be NSAIDs, sitz baths, avoiding colonic stimulants (coffee, alcohol, spicy food). Reevaluation by proctologist in 48 hours. Antihemorrhoidal creams can help; one spoonful a day of liquid vaseline in case there's underlying constipation.

If it's been going on for more than 5 days without any decrease in pain levels, the surgical option should be reconsidered.

DDx Bartholinitis, sebaceous cysts, sacrococcygeal cysts, supurated hydroadenitis, folliculitis. Because of its closeness with the peritoneum there's a solid risk of systemic infection or fistulization.

Drainage must ideally be within an OR. Antibiotic/painkiller treatment afterwards, but may not necessarily be admitted into ward unless there's an underlying pathology which may impair the immune system (e.g. diabetes).

Either from above (ingested) or from below (introduced through the anus). It can reach up until the rectal ampulla or all the way through the rectosigmoid junction.

Xray evaluates the presence and location of a foreign body, and most importantly the possible presence of pneumoperitoneum. While an anoscope may suffice for extracting objects within the ampulla, it ideally requires spinal anesthesia (for sphincter relaxation) which means this has to be solved in the operating room nonetheless.

Airway, Breathing, Circulation. Correct hypovolemic status. Stabilize fractures. Get an xray, ascertain whether there's active bleeding, notify Surgical.

Most common presentation is cystitis. If patient complains about repeated instances, perform urine culture + antibiogram before administering empiric treatment. Exact type of antibiotic varies depending on infectology guidelines etc (cephalexin, nitrofurantoin, TMP/SMZ…). Suspected pyelonephritis may require IV antibiotics and thus be admitted.

It's largely a symptom rather than a clinical entity per se. Most you can do is ask for the usual, get a blood work done and refer to the urologist. It's mostly a matter of figuring out when to contact a urologist for surgical evaluation.

Sometimes Xrays aren't needed but never hurts to get one and ascertain urolithiasis; as per usual, an ultrasound in this case is more precise.

If there's no sign of hemodynamic instability, treat the pain and send home with rest, NSAIDs, and to warm the area in question (hyperhydration is no longer recommended). If pain comes back, can't be dealt at home adequately, or resists initial treatment all the way up to opioids, admit into ward.

DDx anuria. Initial treatment should be the urethral insertion of a catheter and hope content comes out. Retry with different sizes, or semirrigid catheters if possible. If it fails, a urologist should perform a cystostomy.

Patient doesn't usually present because of this but rather because of acute urinary retention associated to it (see above). Best you can do is write prescriptions for full blood work with PSA, various ultrasounds (transrectal, renal) and a urologist should eventually figure out how to continue treatment for it.

Biggest signs are pain that does not go away by elevating the testicle and the epididymis facing anteriorly. Ecodoppler ultrasound is crucial here, but when strongly suspected one should attempt to manually de-rotate it. Notify Urology and surgical team immediately as this is a very time-sensitive issue and may lead to quite dangerous consequences.

Very sudden and peculiar clinical presentation. Initiate wide-spectrum antibiotics and prep for urgent surgery as soon as suspicion of necrotizing perineal infection appears. Patient may need colostomy, reconstruction, cystostomy, and so on depending affected tissues.

If it's closed renal trauma, get a CT and run hematocrit every two hours to evaluate whether or not there's a progressive hematoma. If so, immediate surgery.

After a CT scan that ascertains the damage is distal to the kidney, coordinate with urologist for a cystourethrography.

pH-related pathologies are always related to an alteration in respiratory function (respiratory acidosis/alkalosis based on CO2 levels) or metabolic function (metabolic acidosis/alkalosis based on HCO3- levels).

Remember Henderson's formula: H+ = 24(PCO2/HCO3-)

And the anion gap: Na+ - (Cl- + HCO3-)

Normal anion gap values are 8-16. Sometimes laboratory test results will adjust for it.

In short:

• Normal anion gap, normal ABS: No pathology
• Normal anion gap, low HCO3-: Adaptation to respiratory alkalosis - hyperchloremic acidosis.
• Low anion gap: Increase of gammaglobulin, usually by hyponatremia.
• Increased anion gap: If it equals decrease in HCO3- it's metabolic acidosis with normochloremia. If it's more, then it's a preexisting metabolic alcalosis. If it's less, then it's hyperchloremic acidosis which may be compensation of respiratory alkalosis.

With increased gap anion:

• Bad peripheric perfusion, hemodynamic/repiratory failure: Type A lactic acidosis. Emergency.
• Hx of DBT, ketonic breath, hyperglycemia: cosnider diabetic ketoacidosis; request ketonemia, ketonuria.
• Hx of alcohol, visual alterations, abdominal pain: alcohols intoxication. Test for blood methanol.
• Renal insufficiency: Sign of severe renal failure.

If none of these, then the cause isn't as obvious. Check lactic acid in blood just to discard Type B lactic acidosis and search for other toxicological agents.

If (Urinary Na + Urinary K) - Urinary Cl <20, check urinary pH and potassium. This usually indicates a tubular issue. If it's >20, it can be type II tubular acidosis or by severe diarrhea.

Check daily urine output and see if Urinary Cl is >30 mEq/day (chlorine-resistant alkalosis). With Urinary K <30 mEq/day, you're facing severe hypokalemia. Otherwise check for blood renin and blood cortisol values (Cushing, malignant hypertension, cancer…)

If urinary Cl <30, origin is either profuse vomiting, diuretics abuse or sometimes even a villous adenoma.

Acidosis here is the end-result of a decline in alveolar ventilation. Could be PE, respiratory muscle paralysis, airway obstruction, anomalies at the CNS… sometimes even seen in cases where ventilation is mechanically obstructed like Pickwick's or severe scoliosis. Low pH, high CO2, usually high HCO3- for comepnsation. Treat underlying disease and offer respiratory suport.

Respiratory alkalosis on the other hand is due to hyperventilation which in turn reduces PCO2. Anything from sepsis to hepatic insufficiency can cause this. High pH, low PCO2; associated with dizziness, paresthesia, peribuccal numbing. Treat underlying disease¹²⁾.

Come back to this when I learn how to make cute little flowcharts. This one's a doozy.

Anything <3.5mEq/l. Very rare for it to be nutritional, usually by transcelular displacement (metabolic alkalosis, insulin therapy, hyperglycemia, stress-related release of catecholamines), extrarrenal losses (vomiting, diarrhea, etc) or renal losses (diuretics, Cushing's, toluene abuse, chewing tobacco…).

The EKG is very typical, with low voltage and prolonged conduction times.

Replenish orally only if K > 2.5 mEq/L and EKG is largely normal. Intravenously if <2.5 mEq/L or if there's clinic/EKG manifestations: 3-4ampoules of 15mEq/L each in 500ml saline in 4-6 hours, at a speed never greater than 40mEq/h. If K <2 it's 80-100 mEq/h and constant monitoring.

Again, either by transcelular displacement (tumoral lysis syndrome, rhabdomyolysis, …) or renal excretion reduction (Addison's, heparin treatment, Acute oliguric renal failure, chronic renal insufficiency, …). Also a characteristic EKG.

Use beta2-agonists, furosemide, calcium gluconate 10% (if K >7mEq/L or EKG without spiking P wave) - 3 ampoules in 200ml of saline in 12 hours. 50-100 mEq/L sodium bicarbonate can be administered in a slow IV drip.

Usually symptomatic when values are <60mg%. First, make sure there's no underlying renal, hepatic or hormonal cause or if it's been triggered by hypoglycemic medication. Evaluate when was the last time the patient ate - if it's right after a meal one would find disautonomic signs, etc.

You can repenish orally with food-grade sugar or sugary drinks if the patient is lucid. If not, 50ml of hypertonic glucose solution 50%, then continue with 10% dextrose IV and keep glycemia above 100mg% after at least 4 hours.

A decrease in total red blood cell mass. ALWAYS a sign of an underlying disease, never a disease per se. Anamnesis is crucial.

Anemia can be broadly divided in macrocytic anemias (MCV > 100fl), microcytic anemias (MCV < 80fl) and normocytic anemias (MCV 80-100fl).

Cool flowcharts go here. Anemias of note are ferropenic anemias, megaloblastic anemias, and hemolytic [autoimmune] anemias.

Anything below 3.5k/mm3. Neutropenia is neutrophiles below 1.8/mm3 and Lymphopenia is when lymphocytes are below 1/mm3. It can be a consequence of particular treatments (mainly, chemo) or as a sign of an underlying disease.

Ask profusely, particularly for medications the patient may be taking. If associated with other signs, suspect a widespread neutropenic infection. I owe you another cool flowchart.

Lymphopenia is usually a sign of immunodeficiency; if acquired, think AIDS or Hodgkin's lymphoma, sometimes TB.

Defined as fever of >38ºC in two instances or >38.5ºC in a single instance + neutrophils <500/mm3 or <1000 acutely (with an expected decrease by extrapolation) within a week. Get blood work, tests for renal and hepatic function, urine sample, blood culture.

Attempt to locate or deduce infection site and treat accordingly. Admit into ward with Cefepime 2g/8h OR Ceftazidime 2g/8h + Amikacin 1g/24h, all IV, with reevaluation in 72 hours.

If present, investigate cause.

Anamnesis can reveal obstructive etiologies if there's abdominal pain, fever, or history of biliary surgery, or a more generic hepatic disease with jaundice if there's a history of appropriate viral infections, IV drug use, transfuions, hepatic toxicity… Hiperthermia and abdominal signs suggest obstructive etiologies, same if the increase of bilirubin and ALP shoot up with normal (or normalized) protrombin time; whereas an increase of ALT/AST with coagulation impairment that does not normalize itself with Vitamin K.

At the primary care level best you can ask for is an ultrasound¹³⁾. The criteria for admission are mostly by feel.

Clinically divided betweenn acute and chronic (at least six months!), Hepatitis A through E being the hallmark hepatotropic viruses: A and E don't have chronic forms whereas B, C and D can become chronic and lead to cirrhosis.

Mostly confirmed with laboratory findings of high AST/ALT and ALP/Bilirubin that's either normal or doesn't increase as significantly as the transaminases.

Serologic studies: IgM vs Hep A, Anti-C antibodies, HbsAg, HbcAc-IgM. Tests for anti-D antibodies exist but are relatively rare. After that you can request a more comprehensive screening.

There's PrEP and PEP for Hep A and B, and PrEP for B also protects against B. There's no PrEP for C or E.

Hepatitis can be treated in an outpatient manner by dealing with nausea and vomiting while waiting for it to blow over; rarely, patients require rehydration in the ward. Warning signs include alteration of mental state and prolongation of protrombin time that's resistant to normalization with Vitamin K: these are signs of sudden hepatic failure.

Chronic hepatitis should be refered to an infectologist, but succinctly: chronic Hep B is treated with IFN and chronic Hep C is treated with IFN + Ribavirin. Late-stage disease often warrants a transplant, but recurrences can still happen.

Clinically characteristic. In here the increase of ALP and Bilirubin is more variable. AST being much higher than ALT is also very characteristic in a lab finding. Provide nutritional support and brace for abstinence symptoms while evaluating the extent of liver damage.

Rapid onset of hepatic disfunction (jaundice, alterations in coagulations) + encephalopathy + no immediate history of liver disease. Try to ascertain if this is the result of pharmacological toxicity (e.g. paracetamol overdose) or anything else that may speed up the etiological diagnosis. Shove into ICU immediately and hope that the liver transplant pulls up quickly enough.

Sudden impairment of renal function, with retention of nitrogen end-products and and increase of either 25% of basal creatinin (with creatinie >2mg%) or 30% (usually a net of 0.5-1mg%). Basal creatinin above 2mg% in previously healthy patients or a straight up doubling of creatinin is enough to ascertain failure; anything above 3 or 3.5mg% is right out.

If creatinin has already been increased, it might be chronic renal failure onto which acute failure has been superimposed. Ultrasounds, urinalysis, even a biopsy will help establishing a cause (glomerular disease, vascular origin, interstitial disease, acute tubular necrosis…).

When in doubt, admit into ward. Kidneys are a tough subject and without a nephrologist around you're going to find yourself hitting the books for a while.

If it presents suddenly it would be wise to ask for diagnostic paracentesis and calculate the Albumin Sero-Ascitic Gradient. If >=1.1 then it's secondary to portal hypertension, most likely caused by cirrhosis: admit, no sodium diet, fluid restriction if Na<115, then provide diuretics in increasing dosage: Spironolactone 100→400mg/d, Furosemide 40→160mg/d. If <1.1, the cause is elsewhere, probably oncologic, and treatment must be specific.

The target is to lose 0.5-1kg/d and ascertain absence of infection. No need to wait for the ascitis to disappear completely before discharging the patient. If the target can't be reached, a therapeutic paracentesis may be required to evacuate the liquid; same if the ascitis is causing difficulty breathing.

Hyperthermia, tachycardia, agtation, signs of cardiac insufficiency (and even atrial fibrilation!), diarrhea/vomiting or even jaundice…

Propranolol 60-80mg/4h. Metimazol 30mg/6h. Iopanoic acid 0.5-1g/24h (to administer one hour after metimazol). iodine solutions (e.g. lugol 10 drops/8h), hydrocortisone 100mg/8h EV.

Except for mycobacterium or fungal infection (which tends to have a more insidious presentation), solid treatment mostly depends on landing an early and specific diagnosis.

Consider possible entry points first: skin infections, Hx of hip/knee replacement surgery, rheumatoid arthritis, diabetes…

Drain sinovial fluid from the affected joint, put in a heparinized tube to test for WBC (>50k!) and another one for Gram staining. Get sinovial fluid culture (in blood culture tubes) and blood culture.

The antibiotic treatment will be defined by age, gram staining results, and the results of anamnesis: Think skin bacteria (S. aureus, S. epidermidis) in IV drug addicts or skin infections, N. gonorrhoeae in sexually active young patients, S. pneumoniae in pulmonary infections, and gram-negative bacteria in the old, infirm, immunosuppression/rheumatoid arthritis.

In short: Vancomicin 1g/12h IV if Gram + coccus (usually staph or strep), Ceftriaxone 1g single dose IV if Gram - coccus (N. gonorrhoeae), and Levofloxacine 500mg/d IV if Gram - bacillus (Ceftazidime 2g/8h IV or Piperacilin 4-5g/6h IV + aminoglucosides if P. aeruginosa).

Vital parameters should improve within 48h, and sinovial volume should halve in 3 to 5 days. Lack of response when diagnosis is certain may imply the presence of hidden infection foci that might require surgical drainage. Meanwhile, drain daily for five days through arthrocentesis (adherences will prevent complete extraction and arthroscopic procedures may be required).

During an acute attack: Indometacin 150mg/d for three days (or any other NSAID available), colchicin (1mg/2h until improvement, signs of toxicity e.g. vomiting/diarrhea, or until a total dose of 6mg), and corticoids (triamcinolone if available, prednisone 20mg/day for 10 days).

To avoid recurrence, 0.5mg/d of colchicin should do it.

No characteristic clinical presentation at the beginning. Sometimes there's palpable purpura, mononeuritis, some vague constitutional symptomatology… in severe cases it can precipitate strokes, organ infarctions or alveolar hemorrhage. Broadly differentiated between large vessel vasculitis (e.g. temporal arteritis, Takayasu's), medium vessel vasculitis (Poliarteritis, Kawasaki's…), and small vessel vasculitis (Wegener's, Churg-Strauss', Schonlein-Henoch's…)

A multisystemic disease with fever and even ischemic symptoms (mainly in young people) with suspicious skin lesions, mononeuritis or even just persistent itching should warrant diagnostic suspicion. Get a blood test with urea, creatinin, chest and paranasal sinuses Xray, blood culture; then HBV, HCV… in fact there's a lot you can reasonably ask for, all the way to cryoglobulins. It stands to reason that I should tell you to start asking just what exactly you can request with the resources at hand.

Treatment is usually a well-calculated dose of prednisone, plus any specific treatment if it comes with Hep B.

Thrombosis associated with the present of Antiphospholypidic antibodies. Usually affects lower limbs and even brain blood vessels leading to ischemic strokes. Also associated with recurrent fetal death.

Treatment is empirical and in a primary care setting only limited to complications.

Either a tendency to coagulate or a tendency to bleed out. Honestly there are a lot of these and would take over half this page.

Usually due to embolism or arterial thrombosis, in practice refers to sudden ischemia of any of the lower limbs. Associated with aneurysms at the abdominal aorta, popliteal artery, plaque ulcerations, heart attack Hx, valve pathology…

Worry when pain begins to *subside*. From pallor to cianosis, coldness to muscular rigidity, pulse loss to gangrene…

Get an ultrasound if and only if it will not impede or delay treatment. Immediately put the affected limb lower than the rest of the body and administer sodium heparin 10kUI in IV bolus + 1kUI IV/h in continuous infusion until KPTT is doubled. Notify nearest vascular surgeon immediately. Do not apply local heat. Do not elevate the affected limb.

Preserve Glasgow and airway. Always supplementary oxygen and monitoring of vital signs.

Adrenaline 0.3-0.5ml IM/SC or IV 1:1000. In pediatrics it's 0.1ml per 10 kilograms, max 0.3ml. Repeat initial dosis every 15-20 minutes. Glucagon if adrenaline fails.

IV fluids to preserve systolic BP above 100mmHg.

Diphenhydramine 25-50mg IV/IM. Bronchodilators. Hidrocortisone 500mg IV or IM to avoid delayed reaction.

Continue monitoring vitals. Ideally you want a 24 hour observational period. If caused by an insect bite or due to IV antibiotics you may benefit in applying a torniquette proximal to the limb for 20 minutes, loosening it for 1 minute.

Patient must continue with antihistamines and corticosteroids after discharge and should probably start carrying epipens.

Strictly defined as sexual assault with penetration.

Lab screen: HIV, HbsAg, Antibody vs. HB core (total), Antibodies vs HBsAg. Test for N. gonorrhoeae, C. trachomatis, trichomones, VDRL, HCG-beta.

Prophylaxis: Ceftriaxone 250mg IM single dose OR Ciprofloxacine 500mg + Metronidazole 2g orally (single dose) + Azithromicin 1g (single dose) OR doxicicline 100mg/12h orally for seven days.

Antiretroviral therapy: Ideally you want the infectologist to decide this one. AZT 300mg/12h + 3TC 150mg/12hn + Efavirenz 600mg/d, for example…

Police intervention: Depends on local laws.

Intramuscular Diclofenac + Dexamethasone. Don't think too much about it. Histories of severe hypertension should get tramadol instead. Evaluate if the patient often shows up with the same symptoms or if it's getting progressive to rule out neurological impairment or a more complicated etiology.

Make sure vascular and nervous function in the affected area is as intact as it can get. Fix it yourself or get a traumatologist. Make sure you can still feel a pulse afterwards, and keep it immobile. Anything more serious than this is a (vascular) surgery affair.sor

Pay attention to them if the patient reports it started suddenly or if they're getting more frequent. Any other sign, particularly BP, should also be checked alongside it. Sudden headaches above the age of 50 should also be evaluated with some care.

Normal painkillers in a quite setting can usually do the trick. If you can ascertain a migraine archetype, ergotamine/sumatriptan/metoclopramide hits the spot in most cases. Jury's out on the effectiveness of carbamazepine for trigeminal neuralgia *once* the pain has already set in. For cluster headaches, administer oxygen, ergotamine and dexamethasone.

For it to be delirium, it must be of sudden onset - otherwise, it'd be dementia (moreso if there's altertaion in orientation and memory!). The presence of hallucinations or delusions is a more schizophrenic affair. Absence of all of this might just be a very dramatic panic attack.

In short, delirium can be mostly hyperactive or hypoactive. The presence of neurological impairment that's seemingly independent from the delirium will suggest the presence of a neurological-based pathology (meningitis, encephalitis, a stroke…).

You either sedate the patient as gracefully as possible or dampen the behavioral changes with haloperidol (0.5-2mg per dose every 6-8hs) or risperidone (0.25-1mg per dose every 8-12 hours) while figuring out and treating the underlying the etiology.

Always secondary to a long, long list of possible etiologies. The rest of the signs and a good anamnesis should give you a rough orientation anywhere from brain tumor to CO inhalation. Treatment is etiological and specific but meanwhile you must ensure a permeable airway (Any patient with Glasgow <8 should be intubated). Sedation must be gentle. Crystaloid saline should always be used except hypoglycemia when glucose solutions can be used. Thiamine goes before dextrose in case alcoholism or severe malnutrition is suspected. Hyperthermia and seizures must be aggressively controlled. Etiological treatment should begin concomitantly.

Ideally you always wanna get a head/brain CT and Xray to cover your ass. A patient otherwise normal that reports consciousness loss of less than five minutes is already worth a discharge. Urgency begins with Glasgow <8 when neurological evaluations begin to fail… not to mention if you can see anisocoria or even CSF leakage. Send to specialist accordingly.

Diminished awareness + papillary edema (good luck evaluating this without the proper tooling!), headaches, and so on. Get a brain CT and at least figure out if it's associated with trauma. It's most likely in the hands of neurosurgeons at that point.

Ask for immediate history of digestive or respiratory disease. It's a peripheric and progressive paresthesia, sometimes painful, which peaks at 4 weeks.

Get a lumbar punction, indicate early physiotherapy, thrombosis prevention, and overall supplementation of impaired functions. It can be treated with plasma donatinos or IV gammaglobulin.

If a patient refers having had a seizure without any alarm sign and its subsequent neurological exam is normal, send to neurologist without specific treatment. The presence of signs warrants at least observation or ward admittance.

Post-critical patients should be evaluated briefly, and those with an actual Hx of epilepsy should at least be asked if they had any change in their usual medication.

A seizure that lasts over 60 seconds should be given Diazepam or Lorazepam at least twice, or IV phenytoin if it looks like grand mal - in which case should be treated and screened fully with special focus in metabolic alterations. Thamine 100mg IV, glucose solution 50% IV, NaCl if needed, CaCl 10ml IV in 10 minutes, Diazepam and Phenytoin… by this point it becomes an ICU situation.

Causes endocranial and endospinal hypertension, plus encephalitic syndrome and your usual infections.

Run tests of pretty much everything, plus a lumbar punction with Gram staining and culture.

If patient <50y, Ceftriaxone 2g/12h IV, dexamethasone 0.6mg/kg/d /6h IV for 2-3 days.

If patient >50y, same but add Ampicilin 2g/4h IV.

Switch to Vancomicin 1g/12h IV + Cefepime/Ceftazidime 2g/8h IV if there's immune suppression, Hx of head trauma or surgery.

Professionals directly involved with the patient can take a single Ciprofloxacin 500mg dose if there's confirmation of meningococcus.

Airway, Breathing, Circulation… as long as the patient is stable a brain CT without contrast will give you the differential between ischemic and hemorrhagic. If the former, admit into ward and see how it develops by keeping a close eye on preexisting conditions and BP.

Aspirin 300mg/day. No corticoids. Someone down the chain of medical professionals will have to offer fibrinolytic treatment at some point; ideally not you.

Treat hypertension only if MBP >130 and systolic >220. Start with labetalol. Avoid a drop of over 20% of BP.

Admit into ward or ICU. Severity depends on size (cutoff of ~3cm) and whether it's above or below the tentorium.

Usuaully of traumatic etiology. Sudden headaches, sensitivity to light… DDx meningitis, but this one can be easily diagnosed with a brain CT. Observation in ICU is ideal.

Always a sign and never a malady per se. If possible, figure out the cause before ruling it out as a weak blood vessel wall leaking due to nose picking or high blood pressure. Ask when, for how long, if it was one time or more, from one or both nostrils, preexisting conditions, administratino of anticoagulants, facial trauma…

Anatomically categorized between and anterior and posterior. First, clean and evaluate. If anterior, soak a piece of cotton in adrenaline and shove it into nostril, with a 10-15 minute manual compression of the nostril. Posterior bleeding will require a good tamponage of the entire nostril with well-vaselined gauze strips or ghettorig a Foley catheter towards the nasopharynx and inflate. Should be admitted into ward and evaluated for at least two or three days, if bleeding continues it goes straight to surgery.

Peritonsillar, retropharyngeal, lateropharyngeal; usually cellulitis secondary to an infectious process.

Ampicilin-Gentamicin for ten days, dexamethasone 4-8mg IM/12h, surgical drainage. Drainage is possible depending on anatomical accessibility but unless the airway is getting blocked the patient can generally wait for a more comfortable setting to perform the procedure.

A cervical abscess is basically the same as above: an infection of the peripharyngeal spaces. If visible and fluctuant, a single incision may ease symptomatology a lot. Otherwise continue treatment as usual; etiological agent is usually Streptococci, H. influenzae, anaerobic bacteria…

A CT scan will give you invaluable info about size, location and anatomic relations for most major elements.

The presentation is evident, and it sometimes can even lead to subcutaneous emphysema with crepitations all around the larynx and trachea.

If symptoms are mild enough see if it improves with basic measures such as oxygen, corticosteroids, etc. If it gets severe intubate immediately. If intubation becomes impossible, is otherwise obstructed or cervical/facial trauma is too severe, emergency tracheostomy/cricothyroideostomy.

Always suspect this first if onset is sudden and during the day.

Supraglottic foreign bodies will only cause dysphagia, while glottic foreign bodies will add hoarse voice and respiratory impairment. Subglottic locations will usually cause an airway obstruction.

Diagnosis is with whatever methodology is available, ideally upper fibroscopy. Oxygen, hidrocortisone, tracheostomy if absolutely needed; coordinate with ENT for eventual extraction.

Nasal obstructions can sometimes be seen in primary care with rhinoscopy and extracted out with delicate enough tweezers. If not possible, send to ENT.

Ear canal obstructions, barring accumulation of earwax, can almost always be done in a primary care setting. If inorganic, dehydrate with alcohol as long as there are no ear lesions; if organic (e.g. an insect) immobilize with vaseline or alcohol before extraction.

Peripheral or central. Remember signs (nistagmus, muscular tone disorders) and symptoms (difference between vertigo and dizziness, and so on).

Block histamine receptors with Difenhydramine and Meotclopramide. If the neurological status allows it, benzodiazepines. Furosemide if Meniere's disease has been established. Check with ENT and evaluate if the patient can be discharged or should be admitted instead.

Oxygen, hidrocrostisone, difenhydamine, humidify. Intubate only if the cause is extralaryngeal and extubation can be safely performed within seven days (or if caused by an infection that usually eases within seven days). Tracheostomy if things go south.

A CT scan is the best tool in this case. Attempt to guarantee immediate survival in case of craneal fracture. Bleeding through the ear or a retroauricular hematoma may indicate damage of the inner ear by an extension of a temporal bone fracture, i.e. a very severe presentation; don't even touch the ears until everything else is stable and only then find the nearest specialist.

For cervical trauma, get front and profile Xrays of the cervical area. If suspicion of pharyngo-esophageal trauma, esophagography or a esophagoscopy. Ultrasound can find a hidden hematoma as an indicator of insidious bleeding. CT only if the patient is stable enough to do so. Until then, ascertain hemodynamic stability, airway/breathing/circulation, and get as many traumatological second opinions as possible.

If conjunctivitis, wash cul-de-sacs with saline and prescripe tobramicin+dexamethasone eyedrops, one drop/4h for seven days. A handful of kleenex, forbid use of contact lenses. Do not give dexamethasone to diabetic patients.

A subconjunctival hemorrhage can be done by excessive Valsalva, high blood pressure, anticoagulation, use of aspirin… if asymptomatic, it should resolve by itself in 7-10 days.

Blepharitis goes away with cold compresses or, if the punctum is visible and looks like about to explode and drain out, hot compresses. Same as conjunctivitis but administered in eye cream form.

Dacryocystitis (lacrimal sac imflamation) requires ideally a treatment of 1g cephalexin/8h for 7 days + ice compresses.

Foreign bodies can be removed with sufficient creativity. If lodged in the cornea or sclera (a common presentation would be metalworkers using angle grinders without eye protection and getting a handful of shrapnel in the face as a result) it can be carefully removed by pulling it out very carefully with a needle, scooping it out with the bevel facing forwards, and then lightly scraping out any remaining oxide residue.

Keratitis can be dealt with artificial tears, except in welders' keratitis which happens 4-6 hours later with severe light sensitivity and blepharospasms. Heavily anesthesize topically in the dark with adequate eyedrops and only then examine - treatment is still artificial tears.

Corneal ulcers are either herpetic or non herpetic. Non-herpetic ulcers are covered with antibiotic eye cream and occluded, and reevlauated in 24 hours. Herpetic ulcers must NOT be covered and must NOT be treated with corticosteroids; use aciclovir eye cream every 6h and artificial tears every 2, then reevaluate in 48 hours.

Episcleritis and Iridocyclitis can be usually diagnosed in primary care but the ideal medication for it is too specific for you to have any chance of finding it.

Severe pain, corneal edema, semi-midriatic, non-reactive pupil. Intraocular pressure of above 50 (but I don't think you'll have anything nearby to measure that…). Acetazolamide 250mg/12h; timolol 0.5% + dorzolamide 2% eye drops, one drop/8h; pilocarpin 1% 1 drop/6h.

Get an ophtalmologist quick; it's not likely you'll have any of this medication at hand.

Wash culs-de-sac and fornices continuously for an hour, and anesthetic eye drops every 20 minutes.

An acidic burn has a good prognosis due to the necrosis self-limiting and containing the extent of the damage. An alkali-based burn generally leads to irreparable corneal damage, with a porcelain aspect to it.

An EDTA solution is good for fornices irrigation and then for swabbing the conjunctive tissue with it. Get an ophtalmologist anyway.

Most commonly seen in kids as an anatomical extension of sinusitis. Treat with systemic antibiotics, assume staphylococcus, streptococcus, or haemophilus.

Evaluate intraocular pressure first… somehow. From there DDx is retinal detachment (remain face-up in bed, atropine drops every 12 hours), vascular retinopathies (Prednuisone 80-120mg orally then Prednisone IV every 48 hours, admit…), endophtalmitis (too complicated to easily manage in primary care). Get an ophtalmologist.

Check visual acuity, eye mobility (especially if the patient sees double), intraocular pressure. Blood in the anterior chamber will drain itself with rest at 45º. Complications are usually not urgent (get an ophtalmologist anyway) but a fracture of the orbital floor will require a CT scan and particularly corroborate the integrity of the rectus inferioris.

Penetrating injuries run the risk of endophtalmitis. Don't apply cream if there's a perforated wound! Guess what: get an ophtalmologist.

The eye is a delicate structure which nevertheless contains adequate capabilities for self-repair. However not only specific medication may be hard to come by, but you may not have access to the diagnostic and therapeutic tools required to what would be otherwise very simple procedures. Therefore, get an ophtalmologist.

If it's greyish and smells like rotten fish, it's bacterial vaginosis: Metronidazole 500mg orally every 12 hours for 7 days.

If it's greenish-yellow, foamy and itches all over, it's Trichomonas vaginalis: same treatment.

If it's like lumpy milk and everything is red and burning, it's Candidiasis: Fluconazole 150mg, one capsule a week for two weeks + a single isoconazole vaginal suppository.

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