NG Tube Placement Confirmation

Nasogastric Tube Placement Confirmation

Core Clinical Message

• Radiographic confirmation remains the reference standard for verifying nasogastric (NG) tube position before:
  • Enteral feeding.
  • Administration of medications, fluids, or other substances.
• The tube tip should be clearly visualized below the diaphragm and its course should be assessed for evidence of respiratory tract placement.
• Epigastric auscultation after air insufflation, commonly called the "whoosh test," is unreliable and should not be used alone to establish safe placement.

When Radiographic Confirmation Is Especially Important

• Before initiating feeds or administering medications through a newly placed NG tube.
• In patients with altered mental status, obtundation, impaired airway protection, or inability to report respiratory symptoms.
• When bedside findings are discordant, uncertain, or technically difficult to obtain.
• When pulmonary or tracheobronchial misplacement is clinically possible.

Why Auscultation Is Not Adequate

• Air insufflation over the epigastrium may produce transmitted sounds even when the tube is incorrectly positioned.
• Auscultation lacks adequate specificity for excluding tracheobronchial or pulmonary placement.
• Reported cases include serious complications and fatalities, particularly when feeding or medication administration follows unrecognized malposition.
• A positive "whoosh" sound therefore does not prove that the tube is in the stomach.

Bedside Adjuncts

Aspirate pH Testing

• A gastric aspirate with a pH of approximately 1 to 5.5 can help exclude pulmonary placement.
• pH testing is not definitive proof of gastric placement in every clinical context.
• Results may be affected by acid-suppressive therapy, enteral feeds, swallowed substances, or inability to obtain an aspirate.
• Use local institutional thresholds and protocols.

Capnography or End-Tidal Carbon Dioxide Detection

• Detection of carbon dioxide can help identify airway or pulmonary placement.
• In comparative intensive care unit data, capnography performed substantially better than epigastric auscultation for discriminating correct from incorrect placement.
• A negative or inconclusive bedside result does not replace radiographic confirmation when the tube will be used for feeding or medication administration.

Ultrasonography

• Ultrasound may provide a rapid bedside assessment in experienced hands.
• It is an adjunct rather than a universal replacement for radiography.
• Operator skill, patient habitus, anatomy, and local validation affect performance.

Decompression-Only Use

• If the tube is used solely for gastric decompression and clearly returns gastric contents, some protocols may allow pH testing or other bedside assessment without routine radiography.
• This approach is context dependent and should follow institutional policy.
• The threshold for radiographic confirmation should be lower when the patient cannot report symptoms, the placement was difficult, or findings are uncertain.

Practical Safety Sequence

1. Insert the NG tube using an appropriate technique and assess the patient for distress, coughing, desaturation, or other concerning symptoms.
2. Do not rely on auscultation alone.
3. Obtain aspirate pH and/or a validated bedside adjunct when appropriate and available.
4. Obtain radiographic confirmation before feeding or administering medications through a newly placed tube, according to local protocol.
5. Reassess if the tube is manipulated, replaced, or the patient's clinical status changes.

Clinical Pearls

• Absence of respiratory symptoms does not exclude malposition, especially in obtunded or neurologically impaired patients.
• A tube that aspirates fluid is not automatically confirmed to be safely positioned.
• The risk of harm comes from instilling feeds or medications into the respiratory tract, not merely from insertion.
• Confirmation is a patient-safety step, not a documentation formality.

Summary Takeaway

• Use radiography as the definitive confirmation method before initiating enteral feeds or administering medications through a newly placed NG tube.
• Never use the epigastric "whoosh test" as the sole method of confirmation.
• pH testing, capnography, and ultrasound can provide useful adjunctive information, but the appropriate method depends on the intended use, patient factors, local protocol, and the reliability of the bedside result.

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Source basis: user-provided evidence summary, including the cited 2020 BMC Gastroenterology comparison of capnography and epigastric auscultation. Follow current institutional policy and applicable professional guidance.

Rapidly Progressive Dementia

Identifying Treatable Causes of Rapidly Progressive Dementia

Clinical Takeaway

• In a Dutch prospective multicenter cohort, 95 of 147 adults with rapidly progressive dementia (RPD), or 65%, received a diagnosis classified as potentially treatment-responsive.¹
• Autoimmune encephalitis (AE) was the largest diagnostic group, accounting for 58 of 147 patients (39%) and 58 of 95 treatment-responsive diagnoses (61%).
• This finding supports a rapid, structured search for reversible and immune-mediated causes. It does not mean that every patient with RPD should receive empiric immunotherapy.
• Seizures, mesiotemporal MRI abnormalities, cerebrospinal fluid (CSF) inflammation, and hyponatremia increased suspicion for AE, whereas characteristic cortical or basal ganglia restricted diffusion favored Creutzfeldt-Jakob disease (CJD) in this cohort.
• If AE is highly suspected, the patient meets an appropriate clinical level of evidence, infection has been reasonably excluded, and a diagnosis requiring biopsy is not being considered, expert recommendations support starting immunotherapy before antibody results return.^2,3

What Is Rapidly Progressive Dementia?

• RPD is a syndrome rather than a single disease.
• It is generally defined as progression from symptom onset to dementia within 1 or 2 years. The study used a stricter definition: dementia causing substantial functional interference within 1 year.¹
• Early etiologic classification matters because several immune-mediated, infectious, toxic, metabolic, neoplastic, vascular, epileptic, nutritional, and psychiatric causes may improve with targeted treatment.
• Early recognition of a nonresponsive disorder such as CJD is also clinically important for counseling, infection-control procedures, care planning, and possible trial enrollment.

Study Design

• Design: prospective, multicenter observational cohort.
• Setting: the Netherlands, including the national referral center for neuroinflammation and neuronal autoantibody testing, an academic memory clinic, and nationwide neurology consultations.
• Recruitment: December 2019 through December 2024.
• Screening: 286 patients with suspected RPD were screened; 147 met inclusion criteria.
• Participants:
  • Median age: 67 years.
  • Female: 67 of 147 (46%).
  • Median time from symptom onset to first presentation: 7 weeks.
  • Median follow-up: 33 months.
• Evaluation:
  • Brain MRI was performed in 146 of 147 patients (99%).
  • Paired serum and CSF were tested for neuronal and glial autoantibodies in 146 of 147 patients (99%).
  • Three neurologists with expertise in neurodegenerative or neuroinflammatory disease established final diagnoses by consensus.
  • Autopsy was performed in 8 patients (5%).

Major Diagnostic Findings

Potentially Treatment-Responsive Causes

• Ninety-five of 147 patients (65%) had a diagnosis classified as potentially treatment-responsive.¹
• AE was the most common category:
  • 58 of 147 patients (39% of the full cohort).
  • 58 of 95 patients (61% of the treatment-responsive group).
• Other treatment-responsive categories included additional neuroinflammatory disorders, toxic or metabolic disorders, delirium, central nervous system infection, malignancy, epilepsy, psychiatric disorders, and a dural arteriovenous fistula.

Nonresponsive Causes

• Fifty-two of 147 patients (35%) had a diagnosis classified as nonresponsive.
• The leading categories were:
  • Neurodegenerative disease: 20 of 147 (14%).
  • CJD: 17 of 147 (12%).
• The responsive versus nonresponsive label was based primarily on whether published evidence suggested that disease-specific therapy could produce sustained, clinically meaningful cognitive improvement. It was not an observed treatment-response endpoint for every participant.

Autoimmune Encephalitis Subtypes

• The 3 most common AE subtypes were:
  • Anti-LGI1 encephalitis: 19 of 58 AE cases (33%).
  • Seronegative AE: 11 of 58 (19%).
  • Autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy: 8 of 58 (14%).
• Together, these diagnoses accounted for approximately two thirds of AE-RPD cases.
• Anti-LGI1 encephalitis was especially common when RPD presented with seizures.
• GFAP astrocytopathy was the most common AE subtype among patients without seizures. Psychosis, early movement disorders, cerebellar ataxia, CSF pleocytosis, and characteristic contrast-enhancement patterns should increase suspicion.
• The investigators recommend including GFAP antibody testing in CSF. GFAP testing is not included in every commercial panel, and serum testing alone has limited specificity.

Clinical Clues: AE Versus Other Causes

Seizures

• New-onset seizures at presentation occurred in 20 of 58 AE cases (34%) versus 9 of 89 non-AE cases (10%), with p less than 0.001.¹
• AE accounted for 20 of the 29 patients with RPD and seizures (69%).
• Seizures may be subtle. In the AE group, nonmotor, autonomic, dyscognitive, or faciobrachial dystonic seizures were common, and seizures were missed at the first presentation in 5 of 20 seizure-positive cases.
• A normal initial history does not exclude seizures. Obtain collateral history, review videos when available, and use EEG when suspicion persists.

Cerebellar and Brainstem Findings

• Cerebellar or brainstem findings were more common with non-AE diagnoses than with AE (21% versus 9%).
• Of the 19 non-AE patients with these findings, 11 (58%) had CJD. This is not the same as saying that 58% of all patients with CJD had these findings.
• Movement disorders alone did not clearly separate AE from CJD at first presentation. Timing was more informative: movement disorders tended to occur within 3 months in AE and later in CJD.

MRI

• Mesiotemporal T2/FLAIR hyperintensities were present in 30 of 57 patients with AE who underwent MRI (53%) versus 7 of 89 patients with other diagnoses (8%).
• Restricted diffusion was more common in non-AE conditions (18% versus 4%).
• Restricted diffusion involving at least 2 cortical regions or the caudate or putamen occurred in 7 non-AE patients and no AE patients; all 7 had CJD.
• These patterns were exclusive within this cohort, not universally pathognomonic. MRI must be interpreted with the clinical syndrome, ADC maps, EEG, CSF, and prion testing.

CSF and Laboratory Clues

• CSF pleocytosis and hyponatremia were more common in AE than in other diagnoses.
• Markedly elevated CSF total tau or a high total-tau-to-phosphorylated-tau ratio can occur in AE and should not be treated as specific for CJD.
• CSF real-time quaking-induced conversion (RT-QuIC) was positive only in CJD cases, but it was negative in 3 patients with autopsy-confirmed sporadic CJD. A negative result therefore does not completely exclude CJD when the phenotype and MRI remain compelling.

A Structured Diagnostic Approach

Immediate Assessment

• Establish the tempo, baseline function, medication exposure, toxic risk, immune status, malignancy history, recent infection, travel, and family history.
• Seek collateral history for subtle seizures, faciobrachial dystonic events, psychiatric change, fluctuation, sleep disturbance, autonomic symptoms, and rapid loss of activities of daily living.
• Stabilize seizures, delirium, electrolyte disorders, respiratory compromise, and other immediate threats while the etiologic evaluation proceeds.

Core Testing

• MRI brain with diffusion-weighted imaging, apparent diffusion coefficient maps, FLAIR sequences, and contrast when appropriate.
• EEG, with prolonged or continuous monitoring if subtle focal seizures or nonconvulsive status epilepticus remain possible.
• Lumbar puncture tailored to the differential:
  • Cell count, protein, glucose, cultures, and pathogen testing.
  • Oligoclonal bands and immunoglobulin G index when inflammation is suspected.
  • Paired serum and CSF neuronal and glial antibody testing.
  • CSF GFAP testing when the phenotype is compatible.
  • Prion studies, including RT-QuIC, when CJD is suspected.
• Blood testing should rapidly address common metabolic, toxic, endocrine, nutritional, infectious, and autoimmune causes according to the clinical context.
• Perform malignancy screening when paraneoplastic AE or another neoplastic process is plausible.

When Can Treatment Start Before Antibody Results?

• This cohort did not test an empiric-treatment strategy and cannot prove that all patients with suspected RPD benefit from treatment while antibody results are pending.
• The 2016 clinical AE criteria allow a provisional diagnosis without antibody results. Possible AE requires all of the following:²
  • Subacute progression over less than 3 months of working-memory deficits, altered mental status, or psychiatric symptoms.
  • At least one supportive feature: a new focal central nervous system finding, unexplained new-onset seizures, CSF pleocytosis, or MRI features suggestive of encephalitis.
  • Reasonable exclusion of alternative causes.
• Best-practice recommendations support acute immunotherapy when AE is highly suspected after basic CSF evaluation has reasonably excluded infection and when corticosteroids will not compromise a needed biopsy for primary CNS lymphoma or another inflammatory mimic.³
• Send antibody studies before treatment whenever feasible, but do not wait for results when the clinical criteria and risk-benefit assessment support treatment.
• Do not use a positive serum antibody alone as proof of AE. Interpret the antibody, specimen type, assay, phenotype, MRI, EEG, and CSF together.

Study Strengths

• Prospective and consecutive screening.
• Multicenter and nationwide referral pathways.
• Nearly universal paired serum and CSF antibody testing.
• Direct MRI review and consensus diagnosis by 3 specialist neurologists.
• Median follow-up approaching 3 years, which reduced the risk of premature etiologic classification.

Limitations and Generalizability

• Referral bias is substantial. Erasmus University Medical Center is the Dutch national center for AE and neuronal antibody testing, likely enriching the cohort for immune-mediated disease.
• Typical CJD cases may have been referred less often, creating selection toward atypical CJD and reducing the observed proportion of prion disease.
• The distribution of RPD causes varies by setting. Infection may dominate in other countries or resource settings, while neurodegenerative disease or CJD may predominate in specialized memory or prion centers.
• Only 8 patients underwent autopsy. Although clinicopathologic agreement was complete in those 8, most diagnoses lacked neuropathologic confirmation.
• The study focused on AE. It did not systematically include every biomarker useful for neurodegenerative disease, and formal neuropsychological testing was available in only a minority.
• Clinical and MRI associations are not validated standalone diagnostic rules. They should guide prioritization, not replace a complete differential diagnosis.

Practical Summary

• RPD is a diagnostic emergency because a large fraction of referred patients may have a potentially responsive cause.
• Search early for AE, infection, toxic-metabolic disorders, malignancy, epilepsy, vascular lesions, nutritional deficiency, and other reversible conditions while evaluating for CJD and neurodegenerative disease.
• Seizures, mesiotemporal MRI abnormalities, CSF pleocytosis, and hyponatremia raise suspicion for AE.
• Multiregional cortical or striatal restricted diffusion strongly raises suspicion for CJD, but no single test should be interpreted in isolation.
• Test paired serum and CSF for neuronal and glial antibodies, including CSF GFAP when clinically appropriate.
• Start immunotherapy before antibody results only when accepted clinical criteria are met, infection and major mimics have been addressed, and the patient-specific risk-benefit assessment supports treatment.

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References

1. van Steenhoven RW, Bastiaansen AEM, Kerstens J, et al. Autoimmune Encephalitis as Treatment-Responsive Cause of Rapidly Progressive Dementia: A Multicenter Prospective Cohort Study. Neurology. 2026;106(11):e214933. doi:10.1212/WNL.0000000000214933.
2. Graus F, Titulaer MJ, Balu R, et al. A Clinical Approach to Diagnosis of Autoimmune Encephalitis. Lancet Neurology. 2016;15(4):391-404. doi:10.1016/S1474-4422(15)00401-9.
3. Abboud H, Probasco JC, Irani S, et al. Autoimmune Encephalitis: Proposed Best Practice Recommendations for Diagnosis and Acute Management. Journal of Neurology, Neurosurgery & Psychiatry. 2021;92(7):757-768. doi:10.1136/jnnp-2020-325300.

Educational lecture notes. RPD and suspected autoimmune encephalitis require urgent specialist evaluation. Diagnostic testing and immunotherapy should be individualized to the clinical syndrome and local resources.

Resistant Gram-Negative Infections

Managing Resistant Gram-Negative Infections: IDSA 2026 Guidance

Clinical Takeaway

• The 2026 Infectious Diseases Society of America (IDSA) guidance changes several practical priorities for invasive resistant gram-negative infections in the United States.¹
• Preferred regimens now include:
  • Cefiderocol monotherapy for invasive Stenotrophomonas maltophilia infection, with an explicit warning that the preference rests mainly on susceptibility, pharmacokinetic/pharmacodynamic (PK/PD), and neutropenic animal data rather than comparative clinical outcomes.
  • Sulbactam-durlobactam plus imipenem or meropenem for invasive carbapenem-resistant Acinetobacter baumannii (CRAB) infection.
  • Ceftolozane-tazobactam for pneumonia caused by Pseudomonas aeruginosa with difficult-to-treat resistance (DTR).
  • Aztreonam-avibactam or cefiderocol for invasive New Delhi metallo-beta-lactamase-producing Enterobacterales (NDM-E), with a slight practical preference for aztreonam-avibactam when available.
• These are treatment suggestions for confirmed infection, not automatic empiric choices. Organism identification, antimicrobial susceptibility testing (AST), resistance mechanism, infection site, illness severity, source control, prior cultures, recent antibiotics, and local epidemiology remain decisive.¹

Scope and Evidence Status

• The guidance addresses ESBL-producing Enterobacterales, AmpC-producing Enterobacterales, carbapenem-resistant Enterobacterales (CRE), DTR P. aeruginosa, CRAB, and S. maltophilia.
• The document is focused on United States practice and reflects evidence and expert consensus available through March 1, 2026. IDSA published the online update on July 30, 2026.¹
• It applies to adults and children, but its dosing table provides adult doses only.^1,2
• IDSA did not use GRADE methodology. The literature review was comprehensive but not necessarily systematic. Some recommendations therefore depend heavily on mechanistic, susceptibility, animal, observational, or expert-consensus evidence.¹
• The guidance does not prescribe longer treatment merely because a pathogen is resistant. Duration should generally follow the infection syndrome, response, source control, host factors, and the time at which active therapy began.¹
• Distinguishing colonization from infection is essential, especially for CRAB and S. maltophilia. Treating colonization exposes patients to toxicity and promotes further resistance.¹

Cross-Cutting Bedside Approach

• Before choosing a drug:
  • Confirm that the isolate represents true infection.
  • Identify the infection source and obtain source control.
  • Review organism-level AST and, when available, the beta-lactamase or carbapenemase mechanism.
  • Review cultures from the preceding 12 months and antibiotics received during the preceding 3 months.
  • Account for illness severity, immune status, renal function, allergy history, drug interactions, formulary access, and local susceptibility patterns.
• Reassess empiric therapy when organism identification and AST become available.
• Use IDSA Table 1 for adult dosing and renal adjustment rather than assuming that the labeled dose is optimized for a resistant isolate.²
• Use current CLSI or FDA breakpoints. The 2026 breakpoint table is linked in the guidance.³

AmpC-Producing Enterobacterales

Moderate-Risk Species

• Hafnia alvei is now grouped with Enterobacter cloacae complex, Klebsiella aerogenes, and Citrobacter freundii as having a moderate risk of clinically significant inducible AmpC production.¹
• Historical acronyms such as SPACE or SPICE are unreliable because they obscure species-level differences in AmpC induction.

Treatment Implications

• Cefepime is a preferred option when the cefepime minimum inhibitory concentration (MIC) is 8 micrograms/mL or lower and an ESBL gene has not been identified.¹
• Ceftriaxone, cefotaxime, and ceftazidime are not suggested for invasive infection caused by these moderate-risk species, even when the initial isolate tests susceptible.
• A patient with a nonsevere infection who was started empirically on ceftriaxone may reasonably complete that regimen only if there is clear clinical improvement and adequate source control.
• Piperacillin-tazobactam is not suggested for invasive infection caused by moderate-risk inducible AmpC Enterobacterales. Its apparent in vitro activity may not translate into reliable protection from AmpC hydrolysis.

NDM-Producing Carbapenem-Resistant Enterobacterales

• Preferred options for invasive NDM-E infection are aztreonam-avibactam and cefiderocol.¹
• Aztreonam resists hydrolysis by metallo-beta-lactamases, while avibactam protects it from commonly co-produced serine beta-lactamases.
• IDSA slightly favors aztreonam-avibactam when available because the fixed formulation synchronizes drug exposure and simplifies administration. Direct comparative clinical evidence remains limited.
• If aztreonam-avibactam is unavailable, ceftazidime-avibactam plus aztreonam is a reasonable alternative.
• Eravacycline or tigecycline may be alternatives only for infections that do not involve the bloodstream or urinary tract.
• Cefiderocol is also preferred for NDM-E, but United States surveillance cited by IDSA found lower in vitro activity for cefiderocol than for aztreonam-avibactam against NDM-E. Treatment should follow isolate-specific AST.¹

DTR Pseudomonas aeruginosa

Pneumonia and Other Nonurinary Infections

• Ceftazidime-avibactam, ceftolozane-tazobactam, and imipenem-relebactam are preferred for nonurinary DTR P. aeruginosa infection when the isolate is susceptible.¹
• For pneumonia, ceftolozane-tazobactam is preferred among these agents. This preference is based mainly on observational comparative-effectiveness data and favorable pulmonary PK/PD, not a head-to-head randomized trial.
• Cefiderocol is an alternative for nonurinary infection when resistance or intolerance precludes a preferred beta-lactam.
• If the isolate produces an NDM, VIM, or IMP metallo-beta-lactamase, cefiderocol becomes the preferred agent.
• Once susceptibility to an active newer beta-lactam or cefiderocol is confirmed, routine combination therapy is not suggested.
• Routine nebulized antibiotics are not suggested when an active systemic beta-lactam is available.

Carbapenem-Resistant Acinetobacter baumannii

Preferred Regimen

• Sulbactam-durlobactam plus imipenem or meropenem is the preferred treatment for invasive CRAB infection.¹
• In a randomized trial of 125 patients with CRAB pneumonia or bloodstream infection, sulbactam-durlobactam plus imipenem was associated with 28-day survival of 81% versus 68% with colistin plus imipenem, and clinical cure of 62% versus 40%.¹
• The comparator was not itself a preferred contemporary regimen, so the trial supports the new regimen but does not resolve every comparison with other active agents.

If the Preferred Agent Is Not Immediately Available

• Use high-dose ampicillin-sulbactam, supplying a total of 9 g of sulbactam per day, plus at least one additional agent such as cefiderocol, minocycline, or polymyxin B.
• This is temporary bridge therapy only until sulbactam-durlobactam plus a carbapenem can be started.

Resistance or NDM Production

• If sulbactam-durlobactam resistance or an NDM gene is identified, IDSA prefers a combination of two nonsulbactam agents selected from active options such as cefiderocol, minocycline, polymyxin B, or tigecycline.
• Limited in vitro data suggest that adding sulbactam-durlobactam may enhance cefiderocol activity, but clinical evidence is insufficient. This should not be presented as an established rescue standard.
• Cefiderocol, minocycline, or polymyxin B should otherwise be reserved as combination alternatives when resistance precludes sulbactam-durlobactam or while access is pending.
• Routine nebulized antibiotics are not suggested for CRAB pneumonia.

Invasive Stenotrophomonas maltophilia Infection

First Decide Whether It Is Infection

• Respiratory isolation commonly represents colonization, particularly in patients with chronic lung disease or ventilator dependence.
• True invasive infection can cause substantial morbidity, including bacteremia and hemorrhagic pneumonia in highly immunocompromised patients.

Preferred Therapy

• Cefiderocol monotherapy is the preferred treatment for invasive S. maltophilia infection.¹
• The evidence boundary is critical:
  • Susceptibility approaches 100% in surveillance datasets cited by IDSA.
  • Human-simulated dosing was bactericidal in neutropenic animal models.
  • Human clinical data are sparse, heterogeneous, and not clearly superior to alternative regimens.
  • Small trial subgroups included only a few patients and produced imprecise or unfavorable point estimates.
• The recommendation is therefore a biologically supported expert preference, not proof of superior patient-centered outcomes.

Alternative Therapy

• Aztreonam-avibactam is an alternative, preferably combined initially with a second active agent.
• If aztreonam-avibactam is unavailable, ceftazidime-avibactam plus aztreonam is a reasonable substitute.
• Levofloxacin, minocycline, and trimethoprim-sulfamethoxazole (TMP-SMX) are alternatives only as components of combination therapy during invasive disease. Monotherapy may be considered only after clear, sustained improvement and confirmed susceptibility.
• Among tetracyclines, IDSA specifically favors minocycline. Tigecycline has less useful susceptibility guidance, while eravacycline and omadacycline are not suggested for S. maltophilia because supporting data are sparse or unfavorable.
• Ceftazidime alone is not suggested because intrinsic L1 and L2 beta-lactamases are expected to make it inactive.

Interpreting the Change From TMP-SMX

• The 2026 guidance no longer treats TMP-SMX as the default monotherapy for invasive S. maltophilia infection.
• This does not mean TMP-SMX is universally ineffective. More than 90% of isolates in United States surveillance remained susceptible, but PK/PD studies generally showed bacterial stasis rather than killing, comparative human data were inconclusive, and toxicity requires monitoring.
• A personal practice of routinely avoiding TMP-SMX is therefore not itself an IDSA recommendation. The guidance lists TMP-SMX as a combination-therapy alternative and requires patient-specific assessment.

New Agents: Avoid Overgeneralization

• The 2026 change summary explicitly describes gepotidacin, pivmecillinam, oral sulopenem, intravenous fosfomycin, and aztreonam-avibactam as FDA-approved agents discussed in the update.¹
• Cefepime-enmetazobactam is described separately as an agent whose treatment role was added. The IDSA change summary does not label it as newly FDA approved.
• These drugs are not interchangeable. Several additions mainly expand urinary-tract options, while others are intended for specific resistance mechanisms or invasive infections.
• Approval status, labeled indication, IDSA-suggested use, AST interpretation, and local availability are separate questions and should be checked before prescribing.

Practical Summary

• CRAB: prioritize sulbactam-durlobactam plus imipenem or meropenem.
• Invasive S. maltophilia: cefiderocol monotherapy is preferred, but the evidence is predominantly preclinical.
• DTR P. aeruginosa pneumonia: prefer ceftolozane-tazobactam when susceptible.
• NDM-E: use aztreonam-avibactam or cefiderocol; aztreonam-avibactam has a slight practical preference when available.
• Moderate-risk AmpC Enterobacterales: add H. alvei to the group; prefer cefepime when appropriate; avoid ceftriaxone and piperacillin-tazobactam for invasive disease.
• Across all groups: treat infection rather than colonization, confirm susceptibility and resistance mechanism, achieve source control, and reassess therapy as microbiology evolves.

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References

1. Infectious Diseases Society of America. IDSA 2026 Guidance on the Treatment of Antimicrobial Resistant Gram-Negative Infections. Published July 30, 2026. Evidence current through March 1, 2026.
2. Infectious Diseases Society of America. Table 1: Suggested antibiotic dosing for adults with antimicrobial-resistant infections. 2026 update.
3. Infectious Diseases Society of America. Table 2: 2026 susceptibility breakpoints.
4. Infectious Diseases Society of America. Supplemental material for the 2026 AMR guidance.

Educational lecture notes based on the cited IDSA guidance. Drug selection and dosing require patient-specific clinical judgment, current susceptibility results, organ-function adjustment, and local formulary review.